Umkc Physiology- Exam 1

Front 1

What is the central theme of physiology & body function?

Back 1

HOMEOSTASIS

Front 2

What is Homeostasis?

Back 2

- Central theme of Physiology & body function.
- Ability of the body to remain consistency despite change.
-Keeping body w/in normal limits

Front 3

Fluid homeostasis is _______

Back 3

Fluid homeostasis is VITAL

Front 4

Water accounts for what % of body weight?

Back 4

60%

Front 5

Fluid homeostasis
-What are the 2 spcaes that the body can be divided into?

Back 5

1. Intracellular
2. Extracellular

Front 6

Fluid Homeostasis- Intra/extracellular
-While the volume of spaces is _______ the osmolarity is almost always ______
Solute concentration is always ______

Back 6

-While the volume of spaces is UNEQUAL the osmolarity is almost always EQUAL
Solute concentration is always EQUAL!

Front 7

Fluid Homeostasis- Intra/extracellular
How are dissolved nutrients almost always maintained??
Na+ and K+ content-->?

Back 7

Dissolved nutrients are almost always maintained in DISEQUILIBRIUM!!
(NA+ & K+ CONTENT= NOT EQUAL)

Front 8

Where is the majority of the fluid in the body? Intra or extra?

Back 8

The majority of the fluid is in the cells, INTRACELLULAR- ~40%

Front 9

How much fluid is outside of the cells? and what 2 broken up into?

Back 9

20% of the fluid is Extracellular.
1. Interestital Fluid-15%
2.Blood Plasma-5%

Front 10

What is the order of organization of the body?

Back 10

CELLS make up TISSUES, which make up ORGANS, which make up ORGAN SYSTEMS.

Front 11

What are tissues?

Back 11

Tissues are a group of cells with a common purpose

Front 12

What are the 4 types of tissues?

Back 12

1.CT-blood, bone, teeth
2.Nervous-Neurons & Glial Cells
3.Epithelium-Protection, compartment, absorbtion, secreation.
4. Muscle- Cardiac, Smooth, Skeleton

Front 13

What is vital for organelle, cell, tissue, organ & organ system functions?

Back 13

HOMEOSTASIS!!

Front 14

How is homeostasis primarily maintained?

Back 14

By 2 FEEDBACK CONRTOLS/CONTROL SYSTEMS
1.Negative feedback
2.Positive feedback

Front 15

Homeostasis primarily maintained by 2 feedback control systems:
1.Negative feedback control-(ex, info about system)

Back 15

1.Negative Feedback-
ex- Thermoregulation
-Use the majority of the time.
-change in consistency
-Variable changes in 1 direction & the system goes back in the opposite direction

Front 16

Homeostasis primarily maintained by 2 feedback control systems:
2.Positive Feedback-ex. -info

Back 16

2. Positive feedback
Ex.- a.Smooth mm in uterine wall& Post.pituitary (oxytocin)
b.Congestive Heart Failure
-Variable changes in 1 direction and system moves in the same direction

Front 17

What is the keypoint in regulation in negative feedback control of Thermoregulation

Back 17

THe Hypothalamus=comparator

Front 18

Neg. Feeback Control: Thermoregulation:
Variable:
Sensor/Set Point:
Comparator:
Effector:

Back 18

Variable:BODY TEMP
Sensor/Set Point: HYPOTHALAMUS & SKIN/98.6
Comparator: HYPOTHALAMUS
Effector: SKELETAL MUSCLE, BLOOD VESSELS (vasodilation to skeleal mm), &SWEAT GLANDS(capable of brining back to normal)

Front 19

Negative feedback control
-Order of flow and feedback:

Back 19

Variable--> Sensor/Setpoint--> Comparator-->Effector--> Variable

Front 20

Neg. Feedback Control:
Dependent Variable:
Independent Variable:
Set Point:

Back 20

Dependent Variable: OBSERVED
--> VARIABLE (Temp.)
Independent Variable: CONTROLLED/SELECTED
-->TIME
Set Point: Shouldn't see much change from set point,BUT set point can change... ex. sick

Front 21

Positive Feedback Control
Smooth MM in Uterine wall & Post. Pituitary (Oxytocin)
Order?

Back 21

Signal-->(Fetal Head streches cervix)-->Variable--> Sensor (CERVIX)-->Effector--> (Uterine Contractions)--> Variable.
- Uterus contracts, hypothalumus releases oxytocin from post. pituitary, and contracts uterus

Front 22

Posititve Feedback Control:
Must be an ____ _____ for all + Feedback control.
Ex. in uterine contractions/... what stops the contractions?

Back 22

Must be an OFF SWITCH for all + feedback control.
Ex. When baby is born uterine contractions stop

Front 23

Cardiac Output =

Back 23

SV x HR= 5L/min/ventricle

Front 24

Cardiac Output is an example of what feedback system if loss in blood?

Back 24

Both + and -

Front 25

If you lose 1 litter of blood in 1 HR, what happens>

Back 25

The Neg.FB control takes over and your heart returns to normal

Front 26

IF you lose 2+ liters of blood in 1HR what happens?

Back 26

+ FB control- = death point and CHF
-CO decreases if not enough fluid in heart to pump blood
-Voltage gated Na+ K+ - blood clotting.

Front 27

At moment of Hemmorage what happens to the CO?

Back 27

At moment of hemorage, CO decreases, but then the sympathetic nervous system takes over to Increase CO & activatity of Angiotensin= Increase in BP back to normal CO.

Front 28

+ FB Congestive Heart Failure (CHF)
LOOK AT SLIDE 12 OF 1ST PPT.

Back 28

LOOK AT SLIDE 12 OF 1ST PPT.

Front 29

What is the functional importance of hydrophylic phosphate heads and hydrophobic lipid tails?

Back 29

Selective separation of intracellular and extracellular spaces.
(selective permeability)

Front 30

Permeable or non permeable compounds:
Alcohol-

Back 30

PERMEABLE- like all other small, non polar moleclues
( GASES-O2, CO2; Fatty Acids; Urea; Alcohol, water???)

Front 31

Permeable or non permeable compounds:
.Glucose

Back 31

NONPERMEABLE- Like other large ,polar(charged) molecules- (ex. Glucose, Ions,Amino Acids, Proteins)... That can still get across memebrane using transport systems(3)

Front 32

Permeable or non permeable compounds:
Amino Acids

Back 32

NONPERMEABLE- Like other large ,polar(charged) molecules- (ex. Glucose, Ions,Amino Acids, Proteins)... That can still get across memebrane using transport systems(3)

Front 33

Permeable or non permeable compounds:
Gases (O2, CO2)

Back 33

PERMEABLE- like all other small, non polar moleclues
( GASES-O2, CO2; Fatty Acids; Urea; Alcohol, water???)

Front 34

Permeable or non permeable compounds:
Ions

Back 34

NONPERMEABLE- Like other large ,polar(charged) molecules- (ex. Glucose, Ions,Amino Acids, Proteins)... That can still get across memebrane using transport systems(3)

Front 35

Permeable or non permeable compounds:
Urea

Back 35

PERMEABLE- like all other small, non polar moleclues
( GASES-O2, CO2; Fatty Acids; Urea; Alcohol, water???)

Front 36

Permeable or non permeable compounds:
Fatty Acids

Back 36

PERMEABLE- like all other small, non polar moleclues
( GASES-O2, CO2; Fatty Acids; Urea; Alcohol, water???)

Front 37

Permeable or non permeable compounds:
Proteins

Back 37

NONPERMEABLE- Like other large ,polar(charged) molecules- (ex. Glucose, Ions,Amino Acids, Proteins)... That can still get across memebrane using transport systems(3)

Front 38

Integral Proteins -
attached or not attached? exp.

Back 38

Strongly attached to biologicaal membrane ( permanetely)

Front 39

Peripheral proteins are or arent attached?? exp.

Back 39

- they adhere only temp to the membrane in which they are assocaited with. Not attached.. electrostactic

Front 40

What is a glycocalyx/ components

Back 40

-it is the outer surface/coat of a carbohydrate
-external side of cell=sugars
Components-
1.Sugars on external side of cell
2.negative electrical charge outside= overall (-) charge surface & repels one another/ other (-) charges

Front 41

What is the fx of glycocalyx

Back 41

1. Signaling- Cell/cell communication
2. Attachment (adhesion?)- glycocalyx to another glycocalyx of dif cell
3.(protection??)
((((1) charge that repels other negative objects.
(2)Many of the carbohydrates act as receptor substances
for binding hormones, such as insulin; when bound,
this combination activates attached internal proteins
that, in turn, activate a cascade of intracellular
enzymes. (4) Some carbohydrate moieties enter into
immune reactions))

Front 42

What junction has occludens?

Back 42

tight junctions

Front 43

what junction of cell to cell has cadherins?

Back 43

desmosomes

Front 44

what cell to cell junction has connexins made up of connexons?

Back 44

gap junctions

Front 45

What do tight juctions do?
ex of tight junctions

Back 45

Preven movement mostly unregulated movement between cells.
ex: BBB, stomach

Front 46

What do Gap junctions do?
ex.

Back 46

They are electrical synapses that stimulated secreation from one cell to another
( channels for passages of small mole & ions??)
ex: Endocrine organs& smooth muscle cells- intercalted disc
-NA+ and K+ pass through here

Front 47

What do Desmosomes do?
ex of desmosomes

Back 47

-very strong, easily spotted in cells
ex. intercalleted disc

Front 48

What 2 ions are high in intracellular concentrations but low extracellular concentrations?

Back 48

K+ -potassium
Mg++ -magnesium

Front 49

What 3 ions are high in extracellular concentrations but low in intracellular concentrations?

Back 49

Na+ - sodium
Ca++ -calcium
Cl- -Chloride

Front 50

What is the highest fluid level and is it extracellular or intercellular of:
- Na+

Back 50

Na+
EXTRACELLULAR
142 mEq/L

Front 51

What is the highest fluid level and is it extracellular or intercellular of:
K+

Back 51

K+
INTRACELLULAR
140 mEq/L

Front 52

What is the highest fluid level and is it extracellular or intercellular of:
Amino Acids

Back 52

Amino Acids:
INTRACELLULAR
200 mg/dl

Front 53

What is the highest fluid level and is it extracellular or intercellular of:
Glucose

Back 53

Glucose:
EXTRACELLULAR
90 mg/dl

Front 54

What is the highest fluid level and is it extracellular or intercellular of:
Ca++

Back 54

Ca++:
EXTRACELLULAR
2.4mEq/L
- Ca++ is very important--> small change in small concentration = Great Effect

Front 55

What is the highest fluid level and is it extracellular or intercellular of:
Mg++

Back 55

Mg++
INTRACELLULAR
58mEq/L

Front 56

What is the highest fluid level and is it extracellular or intercellular of:
Cl-

Back 56

Cl-
EXTRACELLULAR
103mEq/L

Front 57

What is the highest fluid level and is it extracellular or intercellular of:
Phosphates

Back 57

Phosphates:
INTRACELLULAR
75mEq/L

Front 58

What is the highest fluid level and is it extracellular or intercellular of:
HCO3-

Back 58

HCO3-
EXTRACELLULAR
28mEq/L

Front 59

What is the ph of extracellular fluid?

Back 59

extracellular fluid= 7.4

(intracellular fluid= 7.0)

Front 60

What is the ph of intracellular fluid?

Back 60

Intracellular fluid= 7.0

(extracellular fluid= 7.4)

Front 61

What is diffusion?
does it require energy? source?

Back 61

Diffusion= Random movement down gradient(s)
- NO energy source required

Front 62

What are the determinants of diffusion?
law and 6 determinants
inc the determ. = what to diffusion

Back 62

Fick's Law
J= -DA ([delta] c / [delta] x)
1.Gradients (electrical & chem)
2. Size of particle & # of openings = Inc. size & # = Inc. diff.
3. Temp.= Inc. Temp= Inc. diff.
4.Surface Area= Inc. SA=Inc. Diff.
5. Thickness of barrier= Inc. thick of barrier-= DEC. Diff.
6. Pressure= Inc. pressure= Inc.diffusion.
* SA and #

Front 63

What is saturation of the determinants of diffusion?

Back 63

In certain places
1. # of openings
2. Surface area

Front 64

Simple diffusion:
Selectivitity?
Types of gates?4
---channels? -
Ex.

Back 64

- Most channels are selective
-SOme channels are seletively permeable; they can open and close
Types of gates:
1. ligand gated
2. phosphogated
3. voltage gated
4. stretch or pressure gated
LEAKY Channels- always permeable for ion theyare selective for.. (MOSTLY K+)
ex. through phospholipid bilary and ion channels

Front 65

What is facilitated diffusion?
ex

Back 65

Has carrier proteins
-Spontaneous passage of molecules or ions accross membrane passing through specific TM transport proteins
- change configurationas they move throug h the gate
ex. glucose and AA

Front 66

What are the 2 types of active transport?

Back 66

1. primary active transport- ATPase/pumps- 3
a. Na-K pump; b. Ca++Pump; c. H+pump
2. secondary active transport-involves the use of an electrochem gradient.atleast 2 and energy source= ATP - 2:
-a.Cotransporter(symporters); b. countertransporters(antitransporters)

Front 67

Sodium potassium pump is what kind of Active transport system? and is is importance

Back 67

- 1' & expensive
-Importance- to maintain homeostasis
-creates a net (-) energy for membrane potential.
- moves 2K+ in and 3Na out , thus making it more negative.
- electrogenic= can change the movement of water

Front 68

What type of H+ transporter is found in the apical epithelium of the stomach?

Back 68

-ATPASE- B/C STOMACH HAS HIGH CONCENTRATION OF H+ IONS.

Front 69

The net direction of water movement across a membrane depends on what?

Back 69

The solute concentration!!!!!

(osmosis- aquaporins)

Front 70

What is osmolarity?

Back 70

Osmoles/L of solution or
# of particles/L of solution
Osmolarity= molarity (mol/L) x # of particles/molecule
( compared to osmolality- osmoles/kg of solution)

Front 71

What is tonicity???

Back 71

Describes whether cell will change in size.
- THis determines water movement.
--*ONLY looks at NONpermeable solutes
- get isoTONIC solution at hospitals

Front 72

OSMOSIS:The net movement of water is always to the most_______ _____.

Back 72

OSMOSIS:The net movement of water is always to the most CONCENTRATED COMPARTMENT. ( SOLUTE CONCENTRATION)

Front 73

OSMOSIS:
Tonicity ONLY considers _________ ______.

Back 73

OSMOSIS:
Tonicity ONLY considers --NONPERMEABLE SOLUTES.

Front 74

OSMOSIS:
Tonicity ALWAYS decribes the ______ not the ____.

Back 74

OSMOSIS:
Tonicity ALWAYS decribes the --SOLUTION-- not the CELL. (extracellular solution compared to the cell.)

Front 75

IF you have 300 mOsm NaCL in the cell & 300 mOsm NaCl outside the cell along with 100 mOsm Urea outside the cell you have what osmolarity and tonicity?

Back 75

HYPEROSMOTIC
ISOTONIC -( urea is permeable so dissolves)

Front 76

IF you have 200 mOsm NaCL in the cell & 400 mOsm NaCl outside the cell you have what osmolarity and tonicity?

Back 76

HYPEROSMOTIC
HYPERATONIC

Front 77

IF you have 300 mOsm NaCL in the cell & 100 mOsm NaCl outside the cell along with 200 mOsm Urea outside the cell you have what osmolarity and tonicity?

Back 77

ISOTONIC
HYPOTONIC ( BC ELIMATE UREA BC PERMEABLE)

Front 78

IF you have 200 mM of NaCL in the cell along with 100 mM of urea in the cell and & 100 mM of glucose in the cell .. what is the cell's osmolarity??

Back 78

400 NaCl + 100 Urea + 100 Glucose = 600
(NaCl doubles bc it dissolves in cell)

Front 79

IF you have 200 mM of NaCL in the cell along with 100 mM of urea in the cell and & 100 mM of glucose in the cell ... and cell is placed in a solution of 200mM of urea and 250 mM of NaCl.. what is the solutions osmolarity?
Osmolatrity/ tonicity?

Back 79

200 Urea+ 500 NaCl= 700 (Nacl doubled)
Hyperosmotic
Isotonic-(water moves into and out of cell equally)

Front 80

Vesicular transport.
1. Endocytosis- 2 types
2. Exocytosis-importance

Back 80

1. Endocytosis- into the cell
a. Phagocytosis- (cell eating)- immune system components
b.pinocytosis(cell drinking)- smaller compounds, CDL receptors- allows cholesterol to enter the cell,.
2. Exocytosis-movement to outside of the cell- dependent on important ion that stimulates exocytosis: CALCIUM!!!!!

Front 81

Resting membrane potential:
Intracellular vs. extracellular, the body is in: 3 things

Back 81

1. osmotic equilibrium
2. chemical disequilibrium
3. electrical disequilibrium.
= negative charge

Front 82

Resting membrane potential:
Energy is nessary to _____ charges.
Conductors
insulatros

Back 82

Energy is necessary to SEPARATE charges.
Conductors- anything that allows a charged substance to cross the membrane( ex.ion channels/pumps)
Insulator-separtes charge - concentration differences across the cell membrane that determine the electrical potential (ex. phospholipid bilayer, fat)

Front 83

rmp (Vm or Em) is the difference in ??
All cells are different but the agerage rmp =

Back 83

The charge inside vs. outside of the cell. -
= -90mv

Front 84

Equilibrium potential? (Eion)

Back 84

=What the charge is,,
- the membrane potential ( difference between the charge inside vs. outsdie the cell) when the ELECTRICAL & CHEMICAL forces for an ion crossing the membrane are equal & opposite.

Front 85

There is always a ___ Vm for Na

Back 85

POSITIVE Vm

Front 86

Every ion has an equilibrium potential.. what is an equilibrium potential?

Back 86

- The membrane potential where the electrical gradient's force is equal & opposite the chemical gradient's force pushing the ion the opposit way such that the ion's net flux is ZERO.

Front 87

So, if a K+ channel opens and a cell is at resting Vm , K+ goes _______ the cell.

Back 87

So, if a K+ channel opens and a cell is at resting Vm , K+ goes OUTSIDE the cell.

Front 88

If the Vm was -110 and a K+ channel opened, what would happen?

Back 88

moves inside????

Front 89

If a cell is only permeable to Na+, then it's membrane potential is

Back 89

61mv, but biological membrane is never permeable to just 1 ion!!!

Front 90

Nerst equation of Sodium equilibrium potential?

Back 90

Eion = 61/1 x log ( ion out/ ion in)
ENa+ = 61/1 x log ( 142/ 14)

Front 91

A cell's membrane potential is determined by what 2 things?
but what really determines the charge of the cell?

Back 91

1. the equilibrium potentials of all ions
2. the permeability of the membrane to each of those ions.
BUT, what really determines the charge of the cell is the permability!!! bc if you change the permeability of a cell by changing concentraiotn or introducing a new ion = changes charge of cell!!!

Front 92

The Goldman-Hodgkin-Katz equation acconts for what 3 things?

Back 92

1. ion's charge
2. concentraction gradient
3. membrane's permeability to the ion (LEAK CHANNELS!!!)

Front 93

The maintence of normal resting membrane potential primarily depnds on____, then ___, and lastly ________.

Back 93

The maintence of normal resting membrane potential primarily depnds on_EK+_, then _ENa+__, and lastly the Na+/K+ PUMP.

Front 94

If a membrane's permeability to an ion or the ion concentration changes....

Back 94

MEMBRANE POTENTIAL WILL CHANGE.

Front 95

How can you change the membrane potential?? 2
ex.

Back 95

1. Change the membrane's permeability to an ion (open/close channel, or change activity of an active transporter)
2. Change the ion concentration gradient across the membrane
ex. Hyperkalemia (inc. in blook K+ concentation.)
-Ehrn K+ conc. outside the cell inc. the force of the conc. gradeint is lessened.-->Thus, the electrical gradient doesn't require as much force ( (-) intracellular charge) to oppose it, the equilibrium potential of K+ willl be more (+) than normal, & the cell's membrane potential becomes more (+).

Front 96

At a cell's R.M.P., the equilibrium potentials for Na+, K+, Ca++ (& almost always Cl-) are such that when an ion channel for one of these ions opens.....
B.At rest- what determines the direction that ions move through open channels? ex. K+

Back 96

The ions follow their concentration gradient.!
B.-CONCENTRATION GRADIENT RULES-
EX. at rest more K+ inside, so moves outside

Front 97

3 types of electrical signals in cells?

Back 97

1. Graded vs. Action potentials
2. EPSPs & IPSPs
3. Repolarization, Hyperpolarization, &Depolarization

Front 98

5 types/parts of Action Potentials ( electircal signals in the cell)

Back 98

1.Phases
2. Channels
3. Refractory periods
4. AP propagation
5. Conduction velocity

Front 99

What type of electical signals always the same and do not decrease in strength as they travel along the membrane, all-or-none.

Back 99

Action Potentinals

Front 100

What electrical signals only occur in excitable cells and dont lose strength as they travel?

Back 100

Action potentials!

Front 101

What electrical signal has small changes in membrane potential of variable strength/amplidtude that travel a short distance and lose strength as they traveL??

Back 101

Graded potentials

Front 102

What electrical signals occur in ALL cells and can have a + or - effect?

Back 102

Graded potentials

Front 103

IPSPs and EPSPs are part of what electrical signals?

Back 103

Graded potentials

Front 104

EPSP?

Back 104

Excitatory post synaptic potetnial - more positive as cell changes

Front 105

IPSP?

Back 105

Inhibitory post synaptic potentials- cell becomes more negative.

Front 106

Starting at rest which ion channels, if opened, cause an EPSP?

Back 106

Na+ and Ca+

Front 107

Starting at rest which ion channels, if opened, cause an IPSP?

Back 107

K+ and Cl-

Front 108

Terminology for changes in membrane potential (Vm)
1. Depolarization- Vm

Back 108

1. Depolarization- Vm becomes more positive (less negative). EPSPs

Front 109

Terminology for changes in membrane potential (Vm)
2.Repolarization- Vm

Back 109

2. Repolarization- Vm returns to resting value.

Front 110

Terminology for changes in membrane potential (Vm)
3. Hyperpolarization- Vm

Back 110

3. Hyperolarization- Vm becomes more negative than resting. IPSPs

Front 111

Terminology for changes in membrane potential (Vm)
Order that resting Vm travels: If 0. resting

Back 111

1. Depolarization
2. Repoloarization
3. Hyperpolarization

Front 112

How does lidocaine work?

Back 112

Blocks Na+ channel and becomes more negaitve.

Front 113

What 2 cells do AP occur?

Back 113

1. Muscle cells
2. Nervous Cells

Front 114

What is the threshold and what does it take to reach potential ..

Back 114

Threshold- switch acts when its reached voltage from EPSP depolarizing.. potential... -10-40mv above the resting potential
( the higher the harder.. 50mv harder)

Front 115

Action Potential in a Nerve...
8/9 stages
1. R.M.P.

Back 115

1. R.M.P.
2. EPSP depolarizes membrane.
3. EPSP reaches threshold & causes voltage-gated Na+ channel to open
4.Depolarization; Na+ rushes into the cell, activating more VG-Na+ channels
5. Na+ channels close & slow VG-K+ channels open
6. Repolarization; VG-K+channels open
7. Hyperpolarization; VG-K+ still open.( bc of leak channels bringing back to resting pot.)
8.VG-K+ channels close- (goes more (-) bc trying to reach membrane potential)
9./1. R.M.P.

Front 116

What are the mechanics of the VG-Na+ channel:
2 phases:
1. Activation gate-INFO~
2. inactivation gate- INFO~

Back 116

1. Activation gate- closed at rest, quickly opens at threshold depolarization (so gets done quicker).
2. Inactivation Gate- (very slow)- Slowly begins to close at threshold depolarization.

Front 117

What are the mechanics of the VG-K+ channel:
what is it like in the Na mecahnics?

Back 117

-Single VG begins to open at depolarization, but very slow-- Delayed by the same time as the VG Na+ channel's inactivation gate....
Similar to the inactivation gate of Na, will not open gate until AP reaches Peak!!

Front 118

What is the Absolute refractory period due to?

Back 118

Due to: The VG-Na+ channels' closed inactivation gates.

Front 119

Absolute refractory period is:

Back 119

The interval during which a second AP cannot be initiated, no matter how large a stimulus is applied. This is due to the VG-Na+ channels closed inactivation.
( When it is impossible for a neuron to fire another AP)

Front 120

What is Relative refractory period due to?

Back 120

due to: Hyperpolarization; caused by the high K+ conductanc ( slow VG-K+ channels remain open)

Front 121

Relative Refractory Period is:

Back 121

The interval immediately following during which initiation of a second AP is inhibited, but NOT IMPOSSIBLE. due to hyperpolarization; secondary to the slow vg-K+ channles that remain open.) hard bc lose the EPSP

Front 122

CLINICAL SIGN. OF REFRACTORY PERIODS AND EQUILIBRIUM POTENTIALS... SEE NOTES- SLIDE 12 LECTURE3

Back 122

SLIDE 12-LECTURE 3 MUSCLE WEAKNESS

Front 123

(slide 12-lec.3- refract. periods and equi. potentials- clinical importance)
hyperkalemic- due to?

Back 123

-due to dec. insulin & proponal as well as failing kidneys.
-unable to excrete sufficeint K+. Normal K is less than 6.5 mEq/L.- Extracellular fluid has higher k+ than normal

Front 124

(slide 12-lec.3- refract. periods and equi. potentials- clinical importance)
Connection between incr. extracellular K+ & muscle weakness?

Back 124

-At rest membrane is very permeable to K+ bc of leak channels.
-If K+ is elevated extracellularly the concentration gradient is reduced. THus for a electrical gradient doesn't require as much force (neg. intracellular charge) to oppose it. The equilibrium potential of K+ will be more + than normal and the cells membrane potential will become more positive.

Front 125

(slide 12-lec.3- refract. periods and equi. potentials- clinical importance)
Why are her muscles week?

Back 125

Vm is depolarized . IF depolarized above threshold VG-na+ channnels activation gates are opened, but VG na channels inactivation gates are closed & willl stay closed as long as the cell is depolarized = ACCOMADATION.

Front 126

If the spreading of the AP propagation is bidirectional, why wont the AP go backwards?

Back 126

BC of 2 reasons:
1. Absolute Refractory periods
2. Inactivation gates

Front 127

Conduction velocity is increased by 2 things:

Back 127

1. myelin- + change can't escape through mylenated membrane -nodes of ranvier, guillain barre syndrome, MS
2. Diameter- larger diameter= stronger speed of conduction of velocity of myleinated axons.

Front 128

What are Salatory conduction with nodes of Raniver (mylein)?

Back 128

-Propagtion of AP along myelinated axons from 1 node of Ranvier to the next node, Inc. conduction velocity without needing to incr. diameter of an axon.
-not myleinated, but reinforce AP.

Front 129

Conduction Velocity - THe advatages of mylein? 2

Back 129

1. Node of Ranvier is where AP is reinforced so the charge can move to next node.. and inc. conduction velocity.
2. Don't have to activate NaK atpase if cell is mylenated.. so save a lot of energy

Front 130

Mylein Autoimmune disorders:
1. Guillain barre syndrome
- cell type effected
symptoms
solution?

Back 130

- Peripeheral.- Schwaan cells.
symptoms- muscle weakness.. sensory and motor affects.. Can resolve spontanesouly

Front 131

Mylein autoimmune disorders
2. MS
- cell type effected
symptoms
solution?

Back 131

- Attack on oligodentrocytes. slow developing
- processive decline. -demylination
- no cure

Front 132

Components of a neuron:
Dendrites-

Back 132

move signal to soma

Front 133

Components of a neuron:
soma/cell body

Back 133

Where find most organells of neuron

Front 134

Components of a neuron:
axon hillock

Back 134

Where AP starts- closer to RMP closets to nomal. many more VG-NA channels here

Front 135

Components of a neuron:
axon-

Back 135

Organnelle found here
Greater: Mitochondria

Front 136

Components of a neuron:
Where does the action potential begin? why there?

Back 136

Axon hillock bc many more vg-na channels

Front 137

Components of a neuron:
Synapses can be antomically described as 3 things:

Back 137

1. axodendritic
2. axosomatic
3. axoaxonic- axon & axon

Front 138

Types of synapses: 1. Electrical 2. Chemical;
1. Electrical Synapse- desc. conduction, found where>?
Sensation and 2 advantages- 1 disadvantage

Back 138

- cells are linked by gap junctions (2nm)
-Bidirectional conduction.(from cell A to cell B or Cell be to Cell A... chem synapses cant do this)
-Mainly found in: Muscles-Muscle fibers (smooth, cardiac, not skeleton) and on some NErves.
Sensation- these work together- cells work as a single unit.
advandatage: 1. faster relay/ fater communication
2. far more efficent ( cost less)
disadvantage- not much control

Front 139

Types of synapses: 1. Electrical 2. Chemical;
What sybampse works in sensation as a single unit? and advantages/disadvantages:

Back 139

Electrical synapse
advantage:
1. faster relay/communication
2. far more effiecnt - cost less
Disadvantage:
- not much control

Front 140

Types of synapses: 1. Electrical 2. Chemical;
2. Chemical synapse- desc., nt, conduction.
convergence vs.divergence

Back 140

- Involves NT that bind receptors to excite, inhibit, or modify post-synaptic cell.
->100 NT have not been identified.
-IT is the RECEPTOR not the NT that determines the fx.
-1 way conduction: convergence vs. divergence
Convergence- multiple presynaptic onto 1 post synaptic neuron
Divergence- 1 presynaptic onto multiple post synaptic neurons

Front 141

Types of synapses: 1. Electrical 2. Chemical;
Which one is convergence/ divergence

Back 141

Chemical synapses:
1 way conduction: convergence vs. divergence
Convergence- multiple presynaptic onto 1 post synaptic neuron
Divergence- 1 presynaptic onto multiple post synaptic neurons

Front 142

Types of synapses: 1. Electrical 2. Chemical;
What determines the function in chemical synapses?

Back 142

The RECEPTOR determines the Fx... not the NT.

Front 143

Summary of Presynaptic Events: What is Key in presynaptic events?

Back 143

CA++

Front 144

Summary of Presynaptic Events:Whenever you have a presynaptic membrane there are 3 predictiable things:

Back 144

1. Ca++ VG channels
2. lots of mitochondria
3. NT filled vessicles

Front 145

Summary of Presynaptic Events:Presynaptic region is rich in
2 things:

Back 145

1. mitochondria
2. NT-FIllled Vesicles (cocktails)

Front 146

Summary of Presynaptic Events: Depolarization opens VG-Ca++ channels where?

Back 146

Depolarixation opens VG- Ca++ channels at AXONAL ACTIVE SONES. - ca++ enters in and stiumulate nt vessicle exocytosis

Front 147

Summary of Presynaptic Events: When vg-ca++channels open at the axonal active zones- ca++ enter in a dstiumlates what?

Back 147

Vesicles are exocytosed.
Endocytosis allowys for recycling NT

Front 148

Summary of Presynaptic Events: NT can bind presynaptic receptor ( reuptake) which allow for ? ex

Back 148

Active reuptake of that particular NT..
ex SSRPI - depression- prevents serotonin reuptake

Front 149

Classification of NT:
1. Small molecule, Rapidly-acting-

Back 149

(small and fast)
-Elict acute responses
-final processing occurs: in the axon terminal (where production occurs). Vesicles are docked & ready for realse from presynaptic terminal. ( lots of NT stored & ready for release)
EX. Ach,NE, Dopamine, Glycine, GABA, Glutamate, NO

Front 150

Classification of NT:
2. Neuropeptides; Larger molecules, slower (big & slow)

Back 150

-Effects are: slower, more potent, & more prolonged
-Produced in CYTOSOL & transported down AXON via AXONAL STREAMING.
-Fewer neuropeptides produced & released.
-Ex: LH, ACTH, Vasopressin, Ocxytocin, ANGio2, substance P, Insulin, VIP, neurotensin.
advantages:
1. stronger effects
2. longer effects

Front 151

Symaptic cleft/Space:
lg dec. in velocity= predict___ synapses bc?

Back 151

lg dec. in velocity= a LOT of synapases- bc more synapses= INc. in synaptic delay

Front 152

Symaptic cleft/Space:
What is synaptic delay?

Back 152

How long to move from 1 cell to another

Front 153

Symaptic cleft/Space:
synaptic delay of atleast .5ms between the presynaptic depolarization and the postynaptic response due to:

Back 153

- Ca++ entry for Exocytosis
- presynaptic nt release, diffusion, & postsynaptic receptor activation.
-allows 1 to gauge the complexity of a reglex pathway ( # of synapses).

Front 154

Symaptic cleft/Space:
NT relased into the synapse- bind to what on post- or presynaptic membranes?
and what happens if binds presynaptic postsynaptic?(brief)

Back 154

NT released into the synapse binds to RECEPTORS.
-if presynaptic- recycled &/or inactivated by enzymes in the synapse.
Post Synaptic- ionic or metatropic receptors

Front 155

NT relased into synapse and binds to RECEPTOR on Post synaptic cell:
1. Ionotropic REceptors:
2. Metabotropic receptors:

Back 155

1. Ionotropic receptors- directly affect ion channels
2. Metabotropic receptors- use 2nd messengers to produce cellular effects.- slower in activation, but a lot more powerful bc can activate genes and control which proteins are being produced.

Front 156

WHy must a summation occur on an average presynaptic terminal to reach threshold and fire an AP in a postsynaptic neuron?

Back 156

BC- an AP in the average presynaptic terminal causes the release of nt sufficeitnt to change a cell's vm only .5-1 mv, thus for the postsynaptic neruon to reach threshold & fire an AP, summation must occur

Front 157

Summation of EPSP- necessary?

Back 157

-summation is almost ALWAYs necessary to produce an AP.

Front 158

Types of Summation:
1. Spatial

Back 158

Sparial-simultaneous input from multiple places on neuron

Front 159

Types of summation
2. Temporal-

Back 159

successive dischages from single presynaptic terminal..

Front 160

What 3 things are the excitability of a Neuron Changes in Response to?

Back 160

1. Synaptic input (pre&post synaptic)-dif in types of synaptic input
2. Prolonged Activation- (a. synaptic fatigue, b. longterm potential, c. long-term depression.
3. Changes in membrane permeability, ion concentraion, other chems.

Front 161

Most common to least common synapses:
axosomatic axodendritic, axoaxonic....(not in order here)

Back 161

most common:
1. axondendtetic-lger EPSP to get and EPSP
2. axonsomatic
3. axoaxonic

Front 162

Synapses on both the pre&post synaptic cells will _____ the ____ ______.

Back 162

Synapses on both the pre&post synaptic cells will MODULATE the FINAL EFFECT. ( change in potentail)

Front 163

Synapses on both the pre&post synaptic cells will modulate the final effect ( change in potential) by what ways?3

Back 163

1. Postsynaptic inhibition or excitation
2. Presynaptic inhibition
3. Presnaypic facilitation
(2&3 axoaxonal synapse won't deterimine weather an AP will occur, but influence the AP that is created.

Front 164

Axo-axonal synapses are responsible for____ ______ and ______.

Back 164

Axo-axonal synapses are responsible for PRESYNAPTIC INHIBITION and FACILITATION.

Front 165

what does a change like inhibitory or excitory presynaptic input have on AP

Back 165

Presynaptic Inputs CHANGE AP! All AP do NOT look the same!

Front 166

What is synaptic fatigue and flexor withdraw reflex?

Back 166

Each successive stiumulus is identical but the response is progressively smaller due to PRESYNAPTIC CHANGE.
--- This stablizes the system

Front 167

What is memory dependent upon?

Back 167

Synaptic Plasticity

Front 168

What is synaptic plasticity?

Back 168

Ability of synapse to change- either pre or post synaptically results in neuron..

Front 169

How is memory dependent upon synaptic plasticity?

Back 169

The activity level of a synapse will change its fx or responsiveness- the strength of the synaptic connection.

Front 170

How is memory depenent upon synaptic plasticity in transitioning short term to long term>

Back 170

STRUCTURAL CHANGE- DEPENDENT ON PHYSICAL CHANGE ( Protein synthesis & gene activation.

Front 171

The reason changes occur when from short to long depnds on:

Back 171

1. long term potentiation
2. Long-term depression

Front 172

Changes from short to longeterm memory-
1. Long term potentiation:

Back 172

post-synaptic response to prolonged high frequency activation
-glutamate- NMDA receptor (ligand-gated Ca++ changgels)
-Prolonged (ca++)i elevation inc. protein kinase activity & ...synaptic responsivesness

Front 173

Changes from short to long term memomry
2.Long term depression

Back 173

-postsynaptic response to prolonged low frequency activation. ( uses dif type of receptor, but stil NT-glutamate)
- Glutamate-NT-, AMPA-receptor (less sensititve) (Lig-G Ca++/Na+ channels)
- Slower stimulation associtated with lesser inc. in Ca++i

Front 174

Where does neurogenesis occur?

Back 174

olfactory bolb and hippocampus

Front 175

Common alterations in neruonal excitability... the following increases excitability or decrease excitability:
Alkalosis

Back 175

INcreases excitability

Front 176

Common alterations in neruonal excitability... the following increases excitability or decrease excitability:
acidosis

Back 176

Decreases excitability

Front 177

Common alterations in neruonal excitability... the following increases excitability or decrease excitability:
Anesthetics

Back 177

Decreases excitibality

Front 178

Common alterations in neruonal excitability... the following increases excitability or decrease excitability:
Caffeine & theophylline

Back 178

Increases excitability

Front 179

Common alterations in neruonal excitability... the following increases excitability or decrease excitability:
Increased membrane permeablity to Na+ andCa+

Back 179

Increases Excitablity

Front 180

Common alterations in neruonal excitability... the following increases excitability or decrease excitability:
Hypoxia

Back 180

Decreases Excitability

Front 181

Common alterations in neruonal excitability... the following increases excitability or decrease excitability:
Increased membrane permeability to K+ and Cl-

Back 181

Decreaseses Excitability

Front 182

Common alterations in neruonal excitability... the following increases excitability or decrease excitability:
Increased sensitvity of receptors (upregulation)

Back 182

Increases Excitability

Front 183

Common alterations in neruonal excitability... the following increases excitability or decrease excitability:
Down-regulation of receptors ( decreased senstivity)

Back 183

Decreases Excitability

Front 184

PNS-
Afferent-
Efferent-

Back 184

Afferent- sensory
Efferent-motor

Front 185

CNS includes what 2 things and sub levels?

Back 185

1.BRain
a. Cortical LEvel
b. Subcortical leve- medulla, pns, mesencephalon, hypothalums, thalamus, cerebellum, basal ganglia
2. Spinal Cord

Front 186

PNS
- 2 systems?

Back 186

1. Somatic nervous system- controlls skelteal mm
2. Autonomic Nervous system- everything else

Front 187

What are the 2 types of cells in the nervous system and which one is more populous?

Back 187

1. Neurons
2. Neuroglia (glial cells)
glial cells are more populous than neurons

Front 188

Neurons:
Consists of? 3(4 includin hilock)
- Type of transport-main and 2 sub

Back 188

Neurons consists of:
Dentrites, soma/cell body, and axon
-Axonal Transport-- transport prtoeints from cell body
---> 1. Anterograde (fast ( mitochonidria movement) vs. slow ( movement of neuropeptides & proteins)
--->2. Retrograde

Front 189

Neuroglia ( glial cells) :
What type of celll?
CNS-
PNS-

Back 189

Glial cells= support cells
CNS=
1. Astrocytes- most populous. - important in BBB control. -Supplies nutrients to neurons. -Synapse: have capacity to take up excess NT & K+. -Clean up Dead cells??
2. Oligendrocytes- mylenated axon
3. microglia-phagocytic cells
4 Ependymal cells- line ventricles - facilitate movement of CSF

PNS_
1.Schwann Cells- Peripheralto oligendrocytes.- separates and mainain mylein
2. Satelllite cells- found in nuclei, wrap around cells in PNS

Front 190

Neurogenesis in CNS? 2

Back 190

more in PNS,, but in 2 places inCNS:
1. hipocampus
2. olfactory fold

Front 191

Glial Regeneration in CNS??

Back 191

Yes- brain tumors are due to glial cells not neurons

Front 192

Neurogensis in PNS?
Glial regeneration?

Back 192

Yes, and regeneration is much easier

Front 193

Response of peripheral neuron to axonal injury??/

Back 193

1. agter injury- nucleus moves to the periphery of the soma, Chromatolyis occurs, & axon distal to the injur degenerates.
2, Skeletal m. atrophies, schwann cells proliferate, & axon hopefully grows- slowly penetrating the cord of schwann cells.
3. Successful axonal regeneration & skeletal m. recovery
( however if axon cannot penetrate the cord of schwann cells, the growth is disorganized.

Front 194

What controls skeletal muscle contaction?

Back 194

Efferent division of somatic nervous system

Front 195

The efferent division of the somatic nervous system controls skeletal m. contractions which are the following: 3

Back 195

1. 1' voluntary
2. Only excitatory
3. MONOSYNAPTIC- only 1 neuron & 1 synapse
a. The alpha motor neuron (only neuron) orginates in the CNS & projects to skeletal m. via the ventral root.
b. The alpha motor neuron releases the NT- ACh!!!

Front 196

In the somatic motor system, what is the nt releaseed from the efferent neuron?
What receptor does this NT bind and where is the receptor located?

Back 196

ACh.- which binds to nicotinic receptors (Nm) on the myocyte (motor end plate)

Front 197

When Ach binds to Nm receptor on the myocyte what happens?

Back 197

Nm Receptor elicits contraction.

Front 198

Relaxation of myscles in the somatic motor system occurs when?

Back 198

When ACh releases and activation of Nm receptor stops (only when stop contracting mm.)

Front 199

In the somatic motor system why is regular activation of somatic motor neuron vital?

Back 199

For muscle health and function

Front 200

What type of receptors are nicotonic ACh receptors?
-what does it allow to pass through?

Back 200

Ionotropic receptors (ligand-gated)
-- These receptor is an ion channel that allows BOTH Na+ and K+ to selectively pass through... this is done when the channel is open, both ions move through, according to their equilibrium potentials.. resulting change in potential midway b/t the EK+ & ENa+.

Front 201

How does the nicotonic Ach receptor s ligand gated channel activate & open?

Back 201

2 Ach must bind at the alpha subunit.

Front 202

How does Botulinum Toxin work?

Back 202

Blocks ACh release

Front 203

How does Curare work>

Back 203

Competitive antagonist for ACh receptors

Front 204

What is the sequence of events in Neuromuscular transmission?
7.

Back 204

1. AP travels down motoneuron to presynaptic terminal
2.Depolarization of Presynaptic terminal= Opens Ca2+ channel & Ca2+ flows into the terminal.
3. ACh is extruded into the synapse by exocytosis.
4.Ach binds to its receptors (Nm)on the motor end plate.(myocyte)
5.Channels for Na+ & K+ are opened in the myocyte
6. Depolarization of the myocyte causes AP to be generated in the adjacent muscle tissue.
7. ACh is degraded to choline & acetate by actylcholinesterase (AChE); choline is taken back into the presynaptic terminal on an Na+ choline cotransporter

Front 205

Somatic Motor neurons are EFFERENT Neurons:
2 types

Back 205

1. Alpha motor neuron*
2. Gamma motor neuron

Front 206

Somatic motor Neurons... Transmission at neuromuscular junction can be _____ in _____

Back 206

Transmission at neuromuscular junction can be ALTERED in PATHOLOGIES.

Front 207

Somoatic motor neurons Transmission at neuromuscular junction can be altered in pathologies... Ex:
Myasthenia Gravis- what ds is this?

Back 207

- Autoimmune ds where antibodies attack the nicotinic Ach receptors.

Front 208

The PNS -->ANS is described as 3 things: and has what 2 divisions?

Back 208

ANS-
1. INvoluntary,
2. Excitatory & inhibitory
3. Disynaptic
2 divisons: 1. Sympathetic, 2. Parasympatheric
- 2 divisions generally oppose one abother when they innervate the same tissue.. Each system is tonically active although one system is usually predominate at rest

Front 209

ANS- 2 Divisions:
1. Sympathetic NS- what is is>? what does it do?
What NT controls it?

Back 209

- Sympathetic:
-Fight or Flight
-Can selectively activate effectors or elicit a mass discharge, especially during stress response.
NT: Post synaptic: Noradernegic/Adrenegic ( NE, EPI) .... but cholinergic pre-topost ganglion.

Front 210

ANS - 2 Divsions:
2. Parasympathic ns
what is it? what does it do? what NT?

Back 210

Parasympathetic
- Rest & Digest
- Control mechanisms are almost alwyas specific, activating or inhibiting discrete targets. HOwever, parasympathetic fx can coordinate.
NT: Cholinergic
--* 1' parasympathetics.

Front 211

Both the parasympathetic and sympathetic ns have:

Back 211

1. Preganglionic neurons(Cell bodies in IMLgray column/motor nuclei of granial nerves)
2. Postganglionic neurons- ( cell bodies are outside of CNS)

Front 212

Parasympathetic and sympathetic n.s.: 1.preganglionic neurons- All pregannglionic terminals rease whatNT and binds to what?

Back 212

-Release Ach and Binds to nicotonic reveptors (type Nn). on the post ganglionic beuron.
-nACh receptors are ligand-gated ion channels (ionotropic) that are selective for both Na+ and K+

Front 213

Synaptic trasmission in postganlionic axons occurs at multiple sites were _______ (def.) are adjacent to target cells.

Back 213

Synaptic trasmission in postganlionic axons occurs at multiple sites were VARICOSITIES ( Bulbous enlargements with concentrations of vesicles & mito) are adjacent to target cells.

Front 214

The advantages of having varicosities in postganglionic axons?

Back 214

1. Allows for more cells to work toegether
2. Allows 1 neuron to do more work

Front 215

What division is the sympathertic nervous system in?

Back 215

Thoracolumbar divsion (T1- L3/L4)

Front 216

The sympathertic nervous system in the thoracolumbar divsion route from where the preganglionic axon exits

Back 216

Preganglionic axons exit through the WHITE RAMUS into 1 of the ganglia of the sympathetic chain. Fibers will then either:
1.Synapse w/postgaglionic neurons at that ganglia
2. Pass up or down the sympathetic chain, then synapse w/ a different ganglia
3. Pass through the chain & out a sympathetic nerve where it will synapse in a peripheral sympathetic ganglion (celiac or sup. or inf. messenteric)
EXCEPTION to ALL above: ADRENAL MEDULLA- b/c only the effector w/in sympathetic n.s. that is inervated by a preganglionic neuron. - The Adrenal medulla kind of functions like a postganglionic neuron,(even though it is an organ) bc it releases NE &Epi.

Front 217

In the sympathetic nervous system the preganglionic axons exit through the WHITE RAMUS into 1 of the ganglia of the sympathetic chain. Fibers will then do 1 of 3 things:
What is the exception to all of this?

Back 217

Fibers will then either:
1.Synapse w/postgaglionic neurons at that ganglia
2. Pass up or down the sympathetic chain, then synapse w/ a different ganglia
3. Pass through the chain & out a sympathetic nerve where it will synapse in a peripheral sympathetic ganglion (celiac or sup. or inf. messenteric)
EXCEPTION to ALL above: ADRENAL MEDULLA- b/c only the effector w/in sympathetic n.s. that is inervated by a preganglionic neuron. - The Adrenal medulla kind of functions like a postganglionic neuron,(even though it is an organ) bc it releases NE &Epi.

Front 218

Almost all of sympathetic POSTganglionic terminals release what NT at the synapse w/target cells?
This NT activties 2 different catergories of receptors which are?

Back 218

NE/noradrenaline.

NE activates both:
1. Alpha receptors
2. Beta receptors

Front 219

Almost all of sympathetic POSTganglionic terminals release NE at synapse w/target cells. NE activates both alpha & beta receptors.. what is an exception to this and where is it found (2 places)?

Back 219

EXCEPTION: At Sweat Glands & some skeletal muscle vasculature (blood vessels) Most sympathetic POSTganglionic terminals release ACh... (sounds like parasympathetic, but not, it's sympathetic)

Front 220

What are the cells that release the sympathetic response/hormone when the adrenal medulla is stimulated?

Back 220

Chromaffin cells

Front 221

SYMPATHETIC NS:
When stimulated, the adrenal medulla (chromaffin cells) secretes 80% _______ & 20% _____ into the bloodstream. ___ & ___ then circulate throught the body & activate ________ receptors.
* How does the adrenal medulla fx like?

Back 221

When stimulated, the adrenal medulla (chromaffin cells) secretes 80% EPINEPHRINE(EPI/Adrenaline) & 20% NOREPINEPHRINE (NE/Noradrenaline) into the bloodstream. EPI & NE then circulate throught the body & activate ADRENERGIC receptors.
*AM fxs like post-ganglionic neuron

Front 222

SYMPATHETIC NS:
What is the reason that the adrenal medulla releases more EPI than NE?

Back 222

This is bc the adrenal medulla contains the enzyme, phenylethanolamine-N-methyltransferase (PNMT) which catalyzes the conversion of NE to EPI . (rxn requires cortisol)

Front 223

SYMPATHETIC NS:
At Alpha receptors does EPI of NE have a freater potency?? And What does Alpha1 & Alpha 2 receptors do/ where are they found?

Back 223

-NE has a greater potency at alpha receptors than epi.
-Alpha 1 receptors:) fx -Constricts smooth muscle (Gq Protein, IP3 inc. intracellular Ca++.
found on smooth muscle flow through blood vessels.. if on bv = decr. blood flow
Alpha 2receptors: fx. Block NE release (presynaptic receptor), stimulate lipolysis (Gi protein, decr. adenylyl cyclase, decr. cAMP)
-decr. release of NE=off swich.

Front 224

SYMPATHETIC NS:
NE has a greater potency at alpha receptors than epi..
1.Alpha1 receptor:
2.Alpha 2 receptors:

Back 224

1. Alpha 1 receptors:
fx -Constricts smooth muscle (Gq Protein, IP3 inc. intracellular Ca++.
found on smooth muscle flow through blood vessels.. if on bv = decr. blood flow
2. Alpha 2receptors:
fx. Block NE release (presynaptic receptor), stimulate lipolysis (Gi protein, decr. adenylyl cyclase, decr. cAMP)
-decr. release of NE=off swich

Front 225

SYMPATHETIC NS:
Does Epi or NE have a greater potency at Beta (B) receptors?

Back 225

Generally, EPI has a greater potency at Beta receptors than NE. Epi has slightly greater potency at B1 than NE. NE has very little potency at B2 receptors.

Front 226

SYMPATHETIC NS:
Epi in gernerally has a greater potency at Beta (B) receptors than does NE.
1. B1
2.B2
3. B3

Back 226

*1.B1- Epi slightly greater potency than NE
-Fx: Incr. HR & contractility (force of cardiac contraction= inc. C.O.) - (Gs Protein: inc. adenylyl cyclase, Incr. cAMP.)
*2.B2- (all epi)
Fx: Relax smooth muscle, release FA & glucose (Gs protein: incr. adenylyl cyclase, incr. cAMP)
3. B3- found in adipose tissue, heart ( fx less clear- incr. adenylyl cyclase, incr. cAMP)

Front 227

SYMPATHETIC NS:
Drugs exist that are preselective for the adgregenic receptors:
1. Alpha 1-
2. Alpha 2-
3. Beta 1-
4. Beta 2-

Back 227

1. Alpha 1-Phenylephrine
2. Alpha 2-Clonidine
3. Beta 1- Dobutiamine
4. Beta 2-Terbutaline

Front 228

Synthesis & removal of NE:
Ne that is released by nerve terminals remains active for only a FEW SECONDS before undergoing 1 of 3 things:

Back 228

1. REUptake by Presynaptic terminal ( this is what most NE will do)
2. Diffusion into interstium, then blood.
3. Destruction by monoaminie oxidase or catechol-O-methyl transferase.

Front 229

What is pheochromocytoma?

Back 229

Tumor of the chromaffin cells (adrenal medulla).
-They selectively secreate more NE than Epi bc limit amts of coritosl.. so ppl w/these tumors are mostly sympathetic bc have ne in blood all the time.

Front 230

Synthesis & removal of NE:
What 2 enzymes can degrade/ destruct NE after released into the synapse?

Back 230

1. Monaoamine oxidase (MAO)
2. Catechol-O-methyl transferase (COMT)

Front 231

Synthesis & removal of NE:
How is tyrosine converted to dopa?

Back 231

Tyrosine hydroxidase converts tyrosine into dopa when tyrpsine enters into the cytosol of the cell.

Front 232

Synthesis & removal of NE:
Tyrosine--converted to Dopa Tyr OH-ase in cytosol then Dopa is converted to what via what?

Back 232

Dopa is then converted to Dopamine via dopa decarboxylase

Front 233

Synthesis & removal of NE:
Tyrosine-->Dopa-->Dopamine in cytosol.... Dopamine undergoes what to get into the vesicle? ANd once in vessicle what must be present for NE to be synthesised?

Back 233

Dopamine undergoes secondary active transport into the vesicle.. at this point in the vesicle, DOPAMINE-B-HYDROXYLASE must be present to dsynthesize NE.

Front 234

Why does it take longer to remove NE/EPI secreted from the adrenal medulla. (10-30 sec ....

Back 234

Bc the NTs are flowing through blood and they are at different target locations that is is harderd to respond to get back out.

Front 235

Compared to the Sympathetic NS, the Parasympathetic NS:
1. Preganglionic axons?
2. Preganglionic terminals

Back 235

1. Parasympathetic NS has longer preganglionic axons than Sympathtetic
2. Preganglionic terminals release ACh that binds to nicotinic ACh receptors.

Front 236

PARASYMPATHETIC NS:
-is known as the what division?

Back 236

Craniosacral divison

Front 237

PARASYMPATHETIC NS:
- Is the Craniosavral Division
What do preganglionic parasympathetic axons supply? 3 main areas and via waht nerves?

Back 237

1. Supply the face via: Oculomotor (3), Facial(7), glossopharyngeal (9)
2. Thorax & upper abdomen via: Vagus (10)
3. Pelvic viscera via: S2-S4

Front 238

PARASYMPATHETIC NS:
Postganglionic parasympathetic varicosities release what that bind to what receptors on target cells?

Back 238

Release ACh that binds to Muscarinic ACh receptors on target cell.

Front 239

PARASYMPATHETIC NS:
Muscarinic receptors are always what type of receptors?
What do they do?
how do they compare to ionotrophic receptors?

Back 239

-Always metatrophic (G-protein retceptors/metatrophic.)
-Fx of Muscarinic receptors: 1. constrict smooth muscle, 2. Relax sphincters, 3. Stimulate gladular secreations (gi and respiratory).
-Muscarinic receptors are slower than ionotrophic receptors.

Front 240

How does taking a catecholamine drug that targets a Muscarinic receptor (M1-m5) for the Parasympathetic NS differ from a drug/catecholamine that one takes that targets the sympathetic nervous system>?

Back 240

In the sympathetic nervous sytstem those drugs target a specific location... in parasymp they dont they will just activate or inhibit a response.

Front 241

Other NT released from the ANS:
1. Vessicles containing NE can also release 1 of 2 things and what do they do?

Back 241

1.Vessicles containing NE can also release:
1.ATP- speeds response (inc. speed of effectors response of NE)
OR
2.Dopamine- Modulatory in renal vasculature- (effective at both pre or post ganglions- NE target)

Front 242

Other NT released from the ANS:
2. Vesicles containing ACh can also release 3 things & what do they do?

Back 242

2. Vesicles containing ACh can also release:
1. Supstance P- Vasodilator
2. Enkephalins- inhibits ACh release (-autoreceptors- HELPS to inhibit)
3. VIP- vasodilator (-inhibit peptide)

Front 243

Other NT released from the ANS:
EXVEPTION: Where is it found? parasymp or symp? post or pre ganglionic?
category name- what it does/doesn't do

Back 243

EXCEPTION: In both Parasympathetic & Sympathetic POSTganglionic neurons...
-Nonadgrenergic, noncholinergic Neurons: Fx- Don't relase ACh, NE, or Epi, BUT may release Peptides, NOS, purines, substance P, NYP, VIP.. some not all

Front 244

Brief Parasympathetic target receptors & function:
Muscarinic Receptors-

Back 244

Constrict smooth muscle, relax sphincters, stimulate gladular secreations

Front 245

Brief review: Sympatetic Target receptors and Function:
1. Alpha 1-
2. Alpha 2-
3. Beta 1-
4. Beta 2-
5. Beta 3-
EXCEPTION:

Back 245

1. Alpha 1- ** Constricts smooth muscle
2. Alpha 2- Block NE release (presynaptic receptor)
3. Beta 1- Inc. HR & contractility (found in heart)
4. Beta 2-***Relax smooth muscle***, relase FA & glucose
5. Beta 3- Thermogenesis
EXCEPTION: Muscarinic Receptors are activated ACh by the SNS at sweat glands and very smalll portion of vasculature supplying skin & skeletal muscle.

Front 246

It is expected that the same smooth muscle cell could have a muscarinic receptor to stimulate contraction of smooth muscle and beta 2 receptor to stimulate relazation of smooth muscle, however, it would NOT make since for that same cell to have an alpha 1 receptor- why???

Back 246

Bc if it it didm the PNS and SNS would have the same end effect on the cell

Front 247

PNS of heart -predominant tone what does muscarinic receptors do?

Back 247

Keep HR low.. slow HR, decr conduction. - nothing with contractility...

Front 248

SNS of heart - what does B1/B2 rreceptors do?

Back 248

B1- Increases HR and contractility
B2- Increases coronary blood flow

Front 249

What would happen if cornary blood flow w/ alpha 1 receptors on cornary arteries?

Back 249

Cause vasoconstriction and decrease blood flow.

Front 250

PNS of lungs-predominant tone what does muscarinic receptors do?

Back 250

- Constrics broncial smooth muscle, bc when relaxed we don't need a lot of air flow

Front 251

SNS of lungs - what does B2 rreceptors do?

Back 251

-Relaxes Bronchial smooth muscle

Front 252

PNS of bladder-predominant tone what does muscarinic receptors do?

Back 252

-Constricts detrusor
-Relax sphincter
(IN general pNS contracts lg mm and relaxes smooth mm)

Front 253

SNS of bladder - what does Alpha1/B2/EPI receptors do?

Back 253

Alpha 1- constricts sphincter
Beta2 (EPI)- relaxes detrusor

Front 254

PNS of GI tract-predominant tone what does muscarinic receptors do?

Back 254

Constricts muscle
Relax sphincter

Front 255

SNS of GI tract - what does Alpha1 (NE)/B2(EPI) receptors do?

Back 255

-Alpha 1- constricts sphincter
-Beta 2- relaxes muscle

Front 256

SNS of salivary- what does Alpha1 receptors do?

Back 256

Alpha 1- vasocontriction secrete concentrated saliva ( lots of mucus & enzymes.

Front 257

VASCULAR SMOOTH MUSCLE/BLOOD VESSLES -
SNS Predominates- what does Alpha1/B2I receptors do?

Back 257

A1- vasoconstriction
B2- Vasodiation

Front 258

PNS of Salivary Glands- Predominant tone- what do muscarinc receptors do?

Back 258

Stimulates lots of watery secreations.

Front 259

Agonist-

Back 259

Agonist- Ligand that activates a receptor

Front 260

Antagonist?

Back 260

Antagonist- ligand that blocks the action of another ligand.

Front 261

If Arterial baroreglex is functioning properply, PNS activation & SNS inhibition should cause a reflex which is what?

Back 261

a decrease in ARTERIAL BP!

Front 262

How do afferent pathways get into CNS? Enters spinal cord via the:

Back 262

Enters spinal cord via the: POSTERIOR/DORSAL Roots.

Front 263

How much of sensory info is discarded as irrelevant?

Back 263

Greater than 99% of all sensory info

Front 264

Most of mechanical (touch, pressure, ect) enters spinal cord and travels unilaterally up brainstem before crossing over the other side. Afferent synapses in _____ then to the cortex except for smell.

Back 264

Synapse in the THALMUS

Front 265

Sensory receptors are defined by:

Back 265

The type of energy that it activates a receptor.

Front 266

What are the 5 functional types of Sensory receptors?

Back 266

1. Mechanoreceptors: compresion/stress/pressure ( measure bp, hearing, touch,osmolarity- sensed by mechanoreceptor)
2. Thermoreceptors: cold/warm
3.Nociceptors: Damage-(-thermal, mechanical, chemical. (pain-how activated))
4. Photoreceptors (electromagnetic receptors): Light (retina)
5. Chemoreceptors: ligands (taste, smell)

Front 267

Transduction is?

Back 267

When activate receptor, receptor elicits a change in the cell's membrane potential.. in order to release NT

Front 268

Sensory receptors are specific for a partitcular:

Back 268

Energy type (or modality).

Front 269

Sensory receptors are specific for a partitcular:Energy type (or modality).
1. Activation of any sensory rreceptor changes membrane potential and produces what?

Back 269

Receptor potential- change in membrane potential and energy charge.
- maybe be EPSP (most) or IPSP-eye punch
-If reaches threshold- AP is made

Front 270

The intensity or strength of stimulus perception in sensory nerouns, is determind by 2 things:

Back 270

1. Frequency of AP (temporal summation-
2. # of Receptors activated (spatial summation).

Front 271

Increases in stiumus strength will increase the amplidute of receptor potentials, but this isnt a direct relation ship.. w incr temp. Advantage of sigmoid response?

Back 271

Sigmoiadal response- allows greater sensitivity of min and max end. SO even at small change, body can respond.

Front 272

Adaptation at neuron or receptor is?

Back 272

the physiological change there
- occurs in almost every system in body.
- change in response to continue responsiveness

Front 273

Adaptatoin:
1. Perceptual threshold-
2.Adaption can occur at the ___ or in the _____

Back 273

1. Perceptual threshold- level a stimulus must reach for you to react. As it continues there is a decrease in response.
2. Adaptation can occur at the RECEPTOR or in the NEURON- neuron adapt 1st order to 2nd to 3rd, etc. -

Front 274

A. Adapts quickest? adapts slowest?
B.In response to continual high impulse seensoty stimuli, the response of almost all receptors:

Back 274

PACINIAN CORPUSCLE adpts most quickly. JOint and muscle have slower adaptation.
B. In response to continual high Impulse sensory stimuli, the response of almost all receptors: DECREASE, but to varying degrees.

Front 275

Receptors Classified based on Speed of their ADAPTATION:
2.

Back 275

1.Tonic Receptors
2. Phasic Receptors

Front 276

Receptors Classified based on Speed of their ADAPTATION:2
1. Tonic Receptors- rate? fx? found in?

Back 276

Rate: Adapt slowly to prolonged stimuli (days to weeks to see change/adaptation)
FX:- Code stimulus intensity & duration - Protect muscle from tearing & pain receptors
-Found in: golgi tendo organs, nociceptors, chemoreceptros, baroreceptors

Front 277

Receptors Classified based on Speed of their ADAPTATION:2
2. Phasic Receptors- rate? fx? found in?

Back 277

Rate: Adapt rapidly to stimuli
Fx: Detect onset & offset. - Provide sensitivity to charge
Found in: Pacinan corpuscles, vestibular receptors in the inner ear

Front 278

If you activate mechanoreceptors you can actual diminish what other receptor.. ex. grab toe after stubbing?

Back 278

diminish nociceptors

Front 279

Transmission & Processing of Sensory Info:
-How does the brain identify the type, location, specifics of a stimulus?

Back 279

The Labeled line principle/??

Front 280

Transmission & Processing of Sensory Info:
What is the Label Line Principle?

Back 280

A precise modality activates specific receptors & postsynaptic cells. This info continues on a predicted pathway such that particular kinds of info are conveyed via specific nerve fibers to specific regions of the CNS that are programmed for perception of that modality. ( always goes to same places & predicts that this pathway to the CNS will always happen from same places)

Front 281

Transmission & Processing of Sensory Info:
Arrangement of Neuronal fields- 2

Back 281

1. Receptive Fields- dentrices
2. Stimulatory Fields- axons

Front 282

Transmission & Processing of Sensory Info: Arrangment of Neuronal fields-2:
1. Receptive Field- where is it? what is involved
fx?

Back 282

1. Receptive Field- Region where a single fiber's afferent receptors (primarily on DENDRITES) are located.
-Where sensory info on body can activate 1st order neuron.
-There is often overlap between receptive fields of adjacent neurons.

Front 283

Transmission & Processing of Sensory Info: Arrangement of neuronal fields-2:
2. Stimulatory Field- where is it? what is involved? fx?

Back 283

Stimulatory field- Region receiving neuronal input from a specific fiber( from axons)
- Axon fibers once activated, can further divide hundreds or thousands of times to activate multiple post-synaptic terminals. The neuronal area stimulated by each incoming fiber is its: STIMULATORY (DISTRIBUTION) FIELD.

Front 284

Transmission & Processing of Sensory Info: Facilitatoin vs. Activation of output nerve fibers. Ex. 3 excitatory synapses , which postsynaptic cell is most likely to fire an action potential???

Back 284

The middle - output fiber 2 bc it is in the discharge zone and not the faciliated zone.

Front 285

Transmission & Processing of Sensory Info:
Lateral Inhibition- what does it do mostly;

Back 285

Lateral inhibition- Improves discrimination.

Front 286

Transmission & Processing of Sensory Info:
How does Lateral inhibition improve discrimination?
And 2 Advantages??

Back 286

Sensory stimulation of a single point on the skin can elicit excitation in 1 tract of postsynaptic cells while simultaneously inhibiting lateral neurons. ( 1' neuron response is proportional to stimulus strength-->Pathway closest to the stimulus inhibits neighbors--> Inhibition of lateral neurons enhances perception of stimulus)
Advantages:
1. Decrease the activity going to the brain
2. Allows you to dect sensory info better makes it more precise.

Front 287

Transmission & Processing of Sensory Info:
Lateral Inhibition (Surround Inhibition) is very important centrally:
It occurs throught the CNS and is advantageous since it?

Back 287

Diminishes the lateral spread of excitatory signals.
- Decrease excitation as goes into brain.
-Significantly helps w/localization as occured

Front 288

Transmission & Processing of Sensory Info:
Relay of Signals:3 ways

Back 288

1. Divergence ( 1 source- multiple targets) vs. Convergence ( multiple sources- 1 target)
2. Spontaneously Active Cells
3.Excitation, Inhibition of Spontaneously active cells

Front 289

Transmission & Processing of Sensory Info:
Relay of Signals:
2. Spontaneously Active Cells
- Can be caused by what 2 things and what ways

Back 289

2. Spontaneously Active Cells
Can be caused by/ due to:
A. high permeability to soduium or calcium even when the cell is "at rest"- causes the EPSP
B. Reverbatory (oscillatory) circuits- have own postiive fb... susequent receptors with fb to creat AP

Front 290

Transmission & Processing of Sensory Info:
Relay of Signals:
3. Excitation, Inhibition of Sponteously Active cells- effect of excitation and inhibition of freq. of cont. active beuronal poll. and ap

Back 290

-Effect of excitation & inhibition on the freq. of a continuously active neuronal pool ( due to either continuous neuronal discharge or reverberating circuits).-EFFECT on these cells is to CHANGE the Frequency of AP.
Excitation= Increase AP fire
Inhibition= Decrease AP fire ( won't stop)

Front 291

Transmission & Processing of Sensory Info: Classification of nerve fibers and their respective fx: Myelinated vs. Unmylinated.
1. Myelinated- speed?, Diameter?- general classifications

Back 291

1. Myelinated Nerve Fibers:
= FASTEST NERVE FIBERS
- The larger the diameter= the faster the speed!
General classification: A & C-
A= Mylineated-fast (C=unmyelinated-slow)
A Fibers:
Alpha-fastest, then Beta, then gamma (y), then psio?

Front 292

Transmission & Processing of Sensory Info:
Classification of nerve fibers & fx:
2. Unmylenated

Back 292

Slower & smallest diameter
made up of C fibers

Front 293

Somatic/Touch Receptors:
Types of Mechanoreceptors-6:

Back 293

1.Free Nerve Endings
2. Pacinian Corpuscles
3.Meissner's Corpuscles
4. Merkel's Disks
5. Ruffini's Endings
6. Hair End-Organ

Front 294

Somatic/Touch Receptors:
Types of Mechanoreceptors-6:
1. Free Nerve Endings
-General info-.
a. fx.
b. Location
c.Rate of adaptation:

Back 294

Somatic/Touch Receptors:
Types of Mechanoreceptors-6:
1. Free Nerve Endings
-General info-.More SF portion of skin.
a. fx.-Dectect touch & sensitive to pressure (temp & pain)
b. Location-in Skin, Cornea, Dental Pulp, GI Tract
c.Rate of adaptation- Slow Adaptation- (More Sensitve to constant stimulus)

Front 295

Somatic/Touch Receptors:
Types of Mechanoreceptors-6:
2. Pacinian Corpuscles -General info-.
a. fx.
b. Location
c.Rate of adaptation:

Back 295

2. Pacinian Corpuscles -General info-.LARGEST SENSORY Receptors in the body
a. fx.- Dect deep pressure, vibration ( require greater stimulus
b. Location-In Subcutaneous tissue, Viscera, Joints
c.Rate of adaptation: Rapid Adaptation

Front 296

Somatic/Touch Receptors:
Types of Mechanoreceptors-6:
3. Meissner's Corpuscles
-General info-.
a. fx.
b. Location
c.Rate of adaptation:

Back 296

3. Meissner's Corpuscles
-General info-.Sensitive to rapid adaptation- more SF sensitive
a. fx.- Detect Light Touch & Pressure. ALSO- Great at localization- (particular determining where activation is coming from)
b. Location- on Glabrous Skin
c.Rate of adaptation: Rapid Adaptation

Front 297

Somatic/Touch Receptors:
Types of Mechanoreceptors-6:
4. Merkel's Disks
a. fx.
b. Location
c.Rate of adaptation:

Back 297

4. Merkel's Disks
a. fx.-Localize continous pressure ( can do this bc slow adaptation)
b. Location- ALL Skin
c.Rate of adaptation: Slow Adaptation

Front 298

Somatic/Touch Receptors:
Types of Mechanoreceptors-6:
5. Ruffini's Endings
a. fx.
b. Location
c.Rate of adaptation:

Back 298

5. Ruffini's Endings
a. fx.- Sensititve to stretch or indentation. ALSO_ Proprioception- Where body is in space.
b. Location- Deep Layers of Skin, Joints, Surrounding tooth Roots ( periodontal lig).
c.Rate of adaptation: Slow Adaptation

Front 299

Somatic/Touch Receptors:
Types of Mechanoreceptors-6:
6. Hair End-Organ
a. fx.
b. Location
c.Rate of adaptation:

Back 299

6. Hair End-Organ
a. fx.-hair movement
b. Location- Base of Hair follicle
c.Rate of adaptation: Rapid Adaptation ( to stimuluis)

Front 300

Somatic/Touch Receptors:
Types of Mechanoreceptors-6:
Which types are Rapid adaptation? 3

Back 300

1. Hair End-organ
2.Pancinian Corpuscles
3.Meissner's Corpuscles

Front 301

Somatic/Touch Receptors:
Types of Mechanoreceptors-6
Which types are Slow adaptation? 3

Back 301

1. Free Nerve Endings
2. Merkel's Disks
3. Ruffini's Endings

Front 302

Somatic/Touch Receptors:
Types of Mechanoreceptors-6
Which type is sentisve to stretch or indentation and Proprioception?

Back 302

Ruffini's ending

Front 303

Somatic/Touch Receptors:
Types of Mechanoreceptors-6
Which types are sensitive to more SF pressure/ touch?
Deep?

Back 303

SF- Freen nerve endings & Meissner's corpuscles

Deep-Pacinian Corpuscles

Front 304

Somatic/Touch Receptors:
Types of Mechanoreceptors-6
Which type is found inDeep layers of skin, joints and surronding tooth roots, includes periodontal ligament?

Back 304

Ruffini's endings

Front 305

Somatic/Touch Receptors:
Types of Mechanoreceptors-6
Paired Rapid and SLow adapting at each layer of skin:
What is Meissner's Corpuscle do , is if rapid or slow and who is it paired with and what does it do? Where is this pairing? hairless? hairy skin?

Back 305

Messiner's corpuscle- Rapid- Flutters AND Paired with
MERKEL's Disk- Slow and steady skin indentations.
Paired at very SF layers. ( Messiner's corpsle on hairless skin, Merkel's disk on hairy skin)

Front 306

Somatic/Touch Receptors:
Types of Mechanoreceptors-6
Paired Rapid and SLow adapting at each layer of skin:
What do FREE NERVE ENDINGS do , is if rapid or slow and who is it paired with and what does it do? Where is this pairing? Which is hairy which is hairless skin?

Back 306

Free Nerve Endings- Slow- and detects touch, pressure, temp, pain. Paired with: Hair Follicle Nerve Ending- Rapid, and Flutters.
Found in middle to SF layers of skin. Free N.Endings- Hairless. Hair Follicle- Hairy skin

Front 307

Somatic/Touch Receptors:
Types of Mechanoreceptors-6
Paired Rapid and SLow adapting at each layer of skin:
What is Ruffini's Endings do , is if rapid or slow and who is it paired with and what does it do?Where is this pairing? which is hairless? hairy?

Back 307

Ruffini Ending- Slow- Steady skin Indentation ( hairy skin)
Paired with:
Pacinian Corpuscle- Rapid- Vibration ( Hairless skin)
Found in DEEP layers of skin

Front 308

Somatic/Touch Receptors:
Common Somatosensory Pathways:
The 2 pathways that come into CNS from cutanous sensory systems?

Back 308

1. dorsal column medial Lemniscal pathway
2. spinothalamic pathway

Front 309

Somatic/Touch Receptors:
Common Somatosensory Pathways:
1. Dorsal Column Medial Lemniscal Pathway is responsible for bringing what info into brain?

Back 309

Sensory Pressure and Touch- afferent .

Front 310

Somatic/Touch Receptors:
Common Somatosensory Pathways:
1. What types of fibers are responsible for bringing pressure and touch signals to the brain via Dorsal Column Medial Lemniscal Pathway?

Back 310

Afferent - Quick fibers Alpha-gamma and Alpha-O fibers.

Front 311

Somatic/Touch Receptors:
Common Somatosensory Pathways:
1. Dorsal Column Medial Lemniscal Pathway route? and if signal comes from right side of body, then?

Back 311

It passes up dorsal columns of the spinal cord as ipsilateral afferent information up to the brainstem where it crosses to the other side- contralateral- and goes to thalmus and cortex.If felt on right side, then rigth side of body pressure pain.

Front 312

Somatic/Touch Receptors:
Common Somatosensory Pathways:
How is the spinothalmic pathway different from the Dorsal column medial Lemniscal pathway? 3 ways

Back 312

1. DIfferent in type: Pain and temp. (instead of pressure and touch)
2. Enters in on ipsilateral side, only travels briefely up and dicasates over to other side in spinal cord.
3. Mostly Alpha-O Fibers and C Fibers- so slower paithway

Front 313

Somatic/Touch Receptors:
Common Somatosensory Pathways:
How is the spinothalmic pathway the same from the Dorsal column medial Lemniscal pathway?

Back 313

After it enters and crosses over it still goes through brain stem to thalmus and then into cortex

Front 314

Somatic/Touch Receptors:
Common Somatosensory Pathways:
Why are these 2 dif. pathways important? 2 reasons?

Back 314

1. Bc of the way info travels to brain- Labelled lines
2. Someone who has unilession (1 side of body say right side at the beginning and below that point.)- inability to touch/pressure on right side (delivered into cerebral cortex). on left side have no pain or temp from right side.

Front 315

Proprioception:

Back 315

Awareness of the body's position in space.
conscios vs. unconscions.

Front 316

Proprioception:
A. Static vs. Dynamic

Back 316

A. Static- Know where body is & aware of ti
B. Dynamic- Rate at which our body i moving- less aware of this.

Front 317

Proprioception
B. Receptor types.-4

Back 317

1. Photoreceptors- eyes
2. Touche & Pressure receptors in skin & joints
3. Skeletal Muscle Receptors- (limb, trunk, head)
a. Muscle Spindles-mm length
b. Golgi Tendon Organs
4. Vestibular Receptors- orientation of head & rate at which head is moving

Front 318

Somatosensory Mechanoreceptors in the Mouth & Face- More sensitive than ?
2 types

Back 318

are more sensitive than fingertips.
1. Extensive Innervation
2. Cutaneous &Mucosal Receptors
3. Periodontal Mechanoreceptors

Front 319

Somatosensory Mechanoreceptors in the Mouth & Face- 3 types
1. Extensive Innervation-
a. sensitivity to stimuli
b. Where info revcieved
c. d.

Back 319

1. Extensive Innervation-
a. Increadibly high snsitivity to stimuli
b. Relatively large region of cortex receives info
c. Receptive fields- very small
d. Adaptation- Simulatanelously

Front 320

Somatosensory Mechanoreceptors in the Mouth & Face- 3 types
2. Cutaneous & Mucosal Receptors:
a. 4types
b.other info sent
c.What do mechanoreceptors convey>

Back 320

2. Cutaneous & Mucosal Receptors:
a. Meissner, merkel, ruffni,and Free nerve endings - no pacinian corpuscles
b. Also send Proprioceptive info
c. Mechanoreceptors can vonvey taste perception

Front 321

Somatosensory Mechanoreceptors in the Mouth & Face- 3 types
3. Periodontal Mechanoreceptors
a. location
b. receptors and axon types
c. adaptation

Back 321

3. Periodontal Mechanoreceptors
a. in periodontal ligament
b. 2 receptors: Mostly complex Ruffini- like receptors or 2.Free nerve endings . Axons are large and Myleniated- sensitive to pressure, temp & pain (nociceptors)
c. Adaptation is both SLOW and FAST ( atypical bc normally slow, but here do both)

Front 322

Photoreceptors are sensitive for?

Back 322

for gamma of light and intensity of light

Front 323

Black is seen by cones or rods?

Back 323

rods.. rest by cones????

Front 324

Wavelengths visible to human are are between?

Back 324

400-700nm

Front 325

What happens to light as it passes through a medium of different density? ex 2

Back 325

Light bends
1. concave lens
2. convex lens

Front 326

When light passes through a medium of different density, the light bends:
1. Concave lens-
2. Convex lens-

Back 326

1. Concave lens- Bends outward to project larger...
2. COnvex lens- bends inward to form a FOCAL Point

Front 327

Why is cornea unique?

Back 327

Bc it completely lacks blood flow.
- #1v transplant
-Important bc form tears to here.

Front 328

Optic disc is lacking what?

Back 328

Photoreceptors bc optic nerve = blind spot

Front 329

The fovea is only made of :

Back 329

CONES

Front 330

Retina contains what but where lacks this at optic disk?

Back 330

Retina is that layer that contains photoreceptors.

Front 331

What does the pupil do?

Back 331

Changes the amount of light entering the eye

Front 332

What does the Lens of the eye do?

Back 332

Bends light to focus it on the retina.

Front 333

What is the zonulas?

Back 333

It attaches lens to cilialary muscle

Front 334

What does the Ciliary muscle do>

Back 334

Contraction alters curvature of eye.

Front 335

What place in the eye is filled with fluid and it maintains the struction and shape of the eye to focus?

Back 335

Lens????? or viterous chamber

Front 336

What is the point of the eye that is the focal point of the eye and 1mm square. Mostly made of cones but as you move out the # of cones decreases?

Back 336

Macula

Front 337

Vision- How does the image progected onto the retina? how does brain interperet this?
what is the retina?

Back 337

The image projected onto the retina is upside down, your brain has learned to interpret this as a reversed image.
Retina- inner layer of eye , location of photoreceptors

Front 338

Vision- What controls the amount of light that passes through the pupil?

Back 338

IRIS

Front 339

Vision- the amount of light that passes through the pupil is controlled by the iris:
What is the pupillary Dilator?

Back 339

Pupillary Dilator- Smooth muscle radially oriented around the pupil. (arranged in radiated fashion.)
- Contraction dilates pupil ( allows more light in)
-Stimulated by SNS, and Low Light.- bc u want as much vision into eye as possible- Alpha 1 receptors

Front 340

What type of receptor is involved in pupillary Dilator?

Back 340

an alpha1 receptor- bc causes contraction of smooth muscles

Front 341

Vision- the amount of light that passes through the pupil is controlled by the iris:
What is a Sphincter Muscle:

Back 341

-Smooth muscle circularly oriented aroound the pupil.
- Contraction constrics the pupil
-Stimulated by PNS and by Increase light

Front 342

Why is light bent as it passes through the lens of the eye (convex lens)?

Back 342

To Focus on the Retina!

Front 343

Light bent as it passes through the lens of the eye (convex lens) to focus on the retina.
-What is lens shape contolled by?

Back 343

Lens shape is controlled by CILILARY MUSCLES- which attach via suspensory ligaments (to lens itself) & innervated by PNS.

Front 344

Light bent as it passes through the lens of the eye (convex lens) to focus on the retina.
What kind of structure is the lens? ( tough, elastic, stable, fiberous?) why is it this way? What is this process called?

Back 344

The lens is an ELASTIC structure.
-bc when Ciliary muscles contact- it becomes more spherical ,(soobjects are in focus) and when it relaxes- the lens flatttens and the focal point is further away.Process= ACCOMATDATIOn

Front 345

The lens is an elastic structure so when Cillary muscles contract and relax what happens?

Back 345

Contract-= Lens becomes more spherical and object apear in focus
Relax-= lens flattens & focal point is further away
Process= accomadation

Front 346

What is Presbyopia? when does it happen?

Back 346

Presbyopia- W/age , the lens loses elasticity & kthe ability to accommodate. Thus, the older one gets the more difficult to see CLOSER objects ( bc lens can't thicken up)

Front 347

Ex. Rays of light coming from every point of a DISTANT object are PARALLEL what is the order they pass through in the eye(4) and what does the mind do?

Back 347

Pass through: 1.Cornea, 2. Aqueous Humour, 3. Lens- refract them to a sharp focus upside down and reversed from side to side on 4. RETINA.
The Conscious mind learns to interpret the image and prject it to its true position in space.

Front 348

EX. Rays of light coming i from a NEAR object RADIATE from every point.. what is this do to lens and retina? So Accomodation is?

Back 348

A more convex lens is required to bring these rays to a sharp focus on the retina.
Process of Accommodation: Cillary muscles contract , lens rounds and Object is in focus on the retina.

Front 349

Common vision problems:
Myopia is?
What causes it?
How is it corrected?

Back 349

Myopia- Near-sighted. (Can see close objects but not far away)
-Eyeball is too LONG, so that the image focuses in FRONT of the RETINA.
Corrected by: Concave Lens (bends light outward)

Front 350

Common vision problems:
Hypermetropia is?
What causes it?
How is it corrected?

Back 350

Hypermetropia- Far sighted ( can see far away, but near objects are hard to see)
-Caused by: Eyeball too short, so that the image is focused BEHIND the RETINA
-Corrected W/ convex lens (bends light inward to focal point.

Front 351

Common vision problems:
Astigmatism is?
What causes it?
How is it corrected?

Back 351

Astigmatism- Cornea is not a perfect dome- not problem with lens. Concts are weighted.. differential focal points

Front 352

Common vision problems:
Cataracts are?
What causes it?
How is it corrected?

Back 352

Cataracts- Lens is no longer transparent.. fuzzy, foggy looking through them... surgery

Front 353

Photoreceptors- truely sensitive to light.
- WHree are photoreceptors located? and why?

Back 353

- Located on the periphery of the retina
-thus light must pass through several cells before reaching photoreceptors.

Front 354

1 spot in retina where photoreceptors are exposed?

Back 354

Fovea

Front 355

Photoreceptors are what kind of cells and what do they do?

Back 355

they are bi-polar cells- ganglion cells--> optic nerve. Support cells- That kdo lateral inhibition and horizontal cells defilineated?????

Front 356

Photoreceptors are either ___ or ____.

Back 356

Photoreceptors are either RODS or CONES.

Front 357

Photoreceptors are either RODS or CONES.
Are rods or cones more numerous in the periphery of the retina? and sensitivity?

Back 357

Rods are sensitive to low-intensity light and more numerous in periphery of the retina.

Front 358

.Rods- Sensitive to low-intensity light & more numerous in perifphery of the retina. What is the outersegment of the rod?

Back 358

Outer Segment of Rod- Contains the photopigment (rhodopsin in rods, color pigments in cones) - Membrane shelves line with rhodopsin or colorpigment.

Front 359

.Rods- Sensitive to low-intensity light & more numerous in perifphery of the retina. What is the inner segment of the rod?

Back 359

Innersegment of Rods-
Contains mitochodria, Organelles, and cytoplasm. (responspible for photoreceptors???)

Front 360

Rods- Sensitive to low-intensity light & more numerous in perifphery of the retina. What is the synaptic body of the rod?

Back 360

Synaptic body of the rod- Synapses with either horizontal or bipolar cells.

Front 361

How many photones do you need of light to activate a rod?
a cone?

Back 361

Only need 1 photon of light to activate Rod- bc used in dark lit places.
But, need a ton to activate cones

Front 362

What is Rhodopsin?

Back 362

Light sensitive photopigment.

Front 363

What is Rhodopsin composed of?

Back 363

-Composed of RETINAL (aldhyde form of Vit A, cisform) & SCOTOPSIN (called photopsin in cones)

Front 364

What is the importance of Viatmin A in rhodompsin?

Back 364

Causes night blindess if dificent

Front 365

Rhodopsin- light sensitive photopigment- What happens to light enery?
Key to

Back 365

Light energy quickly ecomposese rhodopsin & retinal swetiches to trans form (which doesnt fit with scotopsin & several intermediary products are formed)
Key-METARHODOPSIN 2- or activated rhodopsin cuases electrical activation of the rods.

Front 366

What in rhodopsin that is the key? THat causes electrical activation of the rods??
route?

Back 366

METARHODOPSIN 2 or Activatred Rhodopsin.
(from bathorhodopsin, lumirhodopisin ,metardopsin 1 to metarhodopsin 2- thencan connect to SCOTOPSIN to form RHODOPSIN... if in cis form.

Front 367

What does photoactivation of rhodpsin cause?? and what happens?

Back 367

Photoactiavation of rhodopsin causes HYPERPOLARIZATION of RODS.--Light decreases membrane Potential!

Front 368

Photoactiavation of rhodopsin causes hyperpolarizations of Rods.--Light decreases membrane Potential!
-->REsting Vm in Photoreceptor cells? Secrete?

Back 368

Resting Vm= ~ -30mV in photoreceptor cells
- These cells tonically secrete NT.

Front 369

Photoactiavation of rhodopsin causes hyperpolarizations of Rods.--Light decreases membrane Potential!
-->Decomposition of rhodopsin activates? what happens?

Back 369

Decomp of rhodopsin activates G-PROTEIN TRANSDUCIN.
-Degrades cGMP
-This in turn closes cGMP-gated NA+ channels--> hyperpolarization.& dec. NT.

Front 370

Photoactiavation of rhodopsin causes hyperpolarizations of Rods.--Light decreases membrane Potential!
-->Rods, Bipolar cells, & horizontal cells use what to relase NT?

Back 370

USE GRADED POTENTIALS- to release NT, don't need AP to do this

Front 371

Different photoreceptors are sensitive to particular wavelengths of light:
Photoactivation is 4 times as fast in ___ compared to ____.

Back 371

Photoactivation is 4 times as fast in CONES compared to RODS

Front 372

Different photoreceptors are sensitive to particular wavelengths of light:
____ are 30-300 times more sensitive to light than _____

Back 372

RODS are 30-300 times more sensitive to light than CONES

Front 373

Most of the population is a:
A. monchromat?
B. Dichromat
C.Trichomat
D.Quadomat

Back 373

TRICHOMAT!s- which means they have 3 cone functions

Front 374

What is a dichromat?

Back 374

Only have 2 functional cones- Red and Green colorblind.

Front 375

What is a monochromat?

Back 375

Lack 3 functional cones

Front 376

Visual pathway:Photoreceptor cells synapse w/ horizontal cells & bipolar cells.
--What are Horizontal Cells?

Back 376

HOrizontal Cellls- Inhibit surrounding cells to increase visual contrast. (lateral inhibition)

Front 377

Visual pathway:Photoreceptor cells synapse w/ horizontal cells & bipolar cells.
--What are Amacrine Cells?

Back 377

Amacrine Cells- Sometimes part of visual pathway- important for definign pathways and important for movement.

Front 378

Visual pathway:Photoreceptor cells synapse w/ horizontal cells & bipolar cells.
--What are Bipolar Cells?

Back 378

Bipolar Cells- Synapse w/ganglion cells. Some depolarize when light hits its receptive field while others will hyperpolarize in response tothe same stimulus

Front 379

Visual Pathways: Axons of ganglion Cells Carry Visual Info Throught the Optic N.:
What type of potentials do ganglion cells utilize to release NT and are constantly active?

Back 379

Ganglion cells use-AP not graded potentials to release nt & are constantly avtive (5-40 AP/sec.).

Front 380

Visual Pathways: Axons of ganglion Cells Carry Visual Info Throught the Optic N.:
Types of Ganglion Cells 3:
A. Wcells
B. XCells
C. YCells

Back 380

Types of Ganglion Cells 3:
A. Wcells-transmit Rod Vision- Lg receptive field, slowest condcution velocity.
B. XCells-Transmit COne &Rode vision, Small REveptive fields, most numerous
C. YCells-Broad Receptive field, fastest condcution velocity, Quick on and off. Important for rapid movement-(like amacrine cell)

Front 381

Visual Pathways:
What carries visual info into the CNS?

Back 381

OPTIC NERVE
-The left cortex receives the right visual field & vice versa.

Front 382

Hearing/Audition
What must happen before a sound can be heard?

Back 382

Air movement must be TRANSDUCED to FLUID MOVEMENT & Fluid movement must be Transxuced to a CHANGE in MEmbrane potential.

Front 383

What does the amplitude of a sound wave determine?

Back 383

Amplitude of a sound wave determines:
INTENSITY (loudness) Lg amplitude= Loud sound

Front 384

What does the frequency of a sound wave determine?

Back 384

PITCH
High frequency= high pitch

Front 385

What does the external ear do for sound waves?

Back 385

Directs the max amount of Sound waves toward the tympanic membrane.

Front 386

What does the tympanic membrane do?

Back 386

Separates the outer and middle ear

Front 387

The Ossicles of the middle ear fx as:

Back 387

Levers to magnify the force of vibration produced at the oval window. (amplifies sound)

Front 388

The ossicles of the mid ear fx as levers to magnify the force of vibration produced at the oval window.
-->What causes Deafness to the middle Ear? 3 things
--> Ossicles can do 3 things

Back 388

Deafness of the Middle Ear:
1. Fusion or damage to ossciles
2. Thickening or damage to Tympanic membrane
3. ELakage of fluid from the inner ear tothe middle ear.
-->Ossicles can uncouple, fuse, thicken of tymponic membrane.

Front 389

What is the tympanic Refleex?

Back 389

Tympanic Reflex: Loud sounds will stimulate this reflex w/in 40-80msec. - Contraction of the Stapedius muscle (connects to stapes) & Tensor Tampi (connects to malleus) will increase the rigidity of the ossicular system. ( Allow sound when contracted help lock bones out)

Front 390

When is the tympanic Reflex mosteffective?
- protects what?
and decrease what?

Back 390

-Most effective for LOW Frequency Sounds
- Protects the Cochlea from Damage & Masks Low freq. sounds
- Decreases detection of one's own speech.

Front 391

Cochlea: What is it? what is it composed of?

Back 391

Cochlea- fluid-filled, hearing component of the inner ear.
composed of: 3 coiled tubes: scala media, scala vestibuli, & scala tympani

Front 392

The basilar membrane is elastic and separates what 2 things in the ear?

Back 392

The Scala tympani and the Media

Front 393

What is the Organ of Corti? (in the ear)

Back 393

-Containing the auditory receptors .. is on the Basilar membrane
-sensitive to movement. sits on basilar membrane. sup. border RE===Tectorial membrane

Front 394

In the ear, the basilar membrane is ____ and the tectorial membrane is more -___.

Back 394

In the ear, the basilar membrane is ELASTIC and the tectorial membrane is more RIGID.

Front 395

ON the organ of corti on the basilar membarne. - containing the auditory receptors... Vibrations of the oval windo cuases?

Back 395

Movement onf the basilar membrane

Front 396

When the basliar membrane (where audiotory receptors are located) vibrates wh hapens to the organ of corti?

Back 396

Hair cells within the organ of corti are stimulated...
This is a mechosenstive- sensitive to streatch.

Front 397

When the basilar membrane vibrates, hair cells w/in Organ of corti are stimulated:
--> Hair cells have ______ that are:

Back 397

Hair cells have STEROCILIA that are project into the TECTORIAL MEMBRANE (rigid plate). - Sterocilia have CATION channels whose gates are linked together and bend in 1 direction - open depolarize.

Front 398

What is the first differentiation of sounds?

Back 398

Frequency

Front 399

The frequency of sound determines what?

Back 399

The portion of the basilar membrane that will vibrate... Allows you to determine pitch.

Front 400

Basilar membrane in the ear takes what to cuse vibration>

Back 400

A LOT OF ENERGY..

Front 401

As frequencies move along the basilar membrane they get 2 things

Back 401

Wider and more flexible! So a low freq sound can enter and cause vibration.

Front 402

When one losese hair cells in ears it cause what to happen? who does this commmonly happen to?

Back 402

Lose the function tovibrate and sound of high pitch frquencies... males tend to lose this.

Front 403

Determination of Loudness of Sound in 3 ways:

Back 403

1. Loud sounds produce sound waves 1/ lg amps, thus they move the oval windo a relatively greaterr distance than quiter sounds.
2. The louder a sound, the greater the # of hair cells that are activated
3. The louder a sound, the faster the rate of AP fired by hair cells.

Front 404

Vestibular System is important forwhat reasons?

Back 404

Important for sensing changes in positoin of the head. - works in cordination with proprioception.

Front 405

Vestibular System is important for sensing changes in positoin of the head.
--> Where are receptors located?
Responsible for?

Back 405

-Receptors are located w/in the inner ear.
-Responsible for relaying info about head position as well as angular acceleration & linear acceleratoin.

Front 406

What are the Utricle and Saccule sensitive to?

Back 406

They are sensitive to head position in space & acceleration in the Horizontal (uticle) & verticle (saccule) planes.

Front 407

What are the Utricle and Saccule are sensitive to head position in space & acceleration in the Horizontal (uticle) & verticle (saccule) planes.
1. The sensory organ?
what is it composed of and what is statconia>

Back 407

Sensory organ= Maculae
Maculae is composed of hair cells embedded in sataconia.
-When the head position changes, the stataconia shifts its position , the hair cell bends and GRADED POTENTIALS are generated. (bottom more mobile thant top. quick movements of head)

Front 408

What is angular accceleration in the ear detected by?

Back 408

detected by sensory receptors in the semicircular canals (ant. post, lat)

Front 409

Angular acceleration is detected by sensory receptors in the semicircular canals.
1. The canals have an expanede base called what that contains what?
2. Hair cells prject into ta gelatinous mass called waht and why>?

Back 409

1. The canals have an expanded base called the AMPULLA (sensory organ for ancular accleration??) containing receptors for angular acceleration
2. Hair cells project into a gelatinous mass called the CUPULA. When the head moves in 1 direction, the bone of the inner ear moves, but the fluid's movement is delayed due to inertia. This causes the cilia to bend, ions to flow, and the hair cells to depolarize.

Front 410

Taste buds contain what? and why is this unusual?

Back 410

Taste buds contain TASTE RECEPTOR CELLS... Unusual bc not neurons, but epithelial cells. Good bc of Hot/cold, last very short time 10days

Front 411

taste buds... Basal cells?

Back 411

Differientatie into taste recetprot cells.

Front 412

Location of taste papillae>

Back 412

tongue, hard & soft palate, pharynx, epiglotis, larynx, stomach, gi, intestine.

Front 413

types of papillae? 5

Back 413

1. circumballate- big post.
2. Foliate
3. fungiform
4.extralingual-everythng, but tongue
5. filiform- tip

Front 414

Categorization of taste stimulants: 1000s of tastes are differentiated primarily based on the activation of:

Back 414

5 different receptors

Front 415

1000s of tastes are differentiated primarily based on the activation of 5 different receptors.. Qualification of receptors:4

Back 415

1. all tastants must dissolve in saliva( have to dissolve in liquid to be able to taste. drymouth cant get taste receptor cells)
2. Individual taste receptor cells may be sensitive to a specific taste stimulus, but may have receptors for multiple taste types. (both sweet & bitter)
3. Olfaction is vital for normal gustation
4. Sweet, bitter, & umami tastes are accounted for by 2 families of taste receptor genes- TR1 & TR2, both of which utiliize the Gprotein gustducin

Front 416

Chemical taste receptor types:
1 Sour taste
- Activated by:
-stimulated by-
Multi canidated receptors signallled by:

Back 416

1 Sour taste
- Activated by: ACID
-stimulated by-H+ - protective taste
Multi canidated receptors signallled by:
a. Amiloride-sensitive epithelial NA+ channel (ENaC), and H+ channels
b. All potential mechanisms lead to depolarization of receptor cells

Front 417

What taste is more strongly linked to salvation and contraction of facial muscles than any other taste in body?

Back 417

SOUR TASTE.
- tongue folds --> acid containing compounds direct away from teeth *** very important reflex for teeth enamel
and salvation--> helps to buffer

Front 418

Sweet taste
a. Stimuli

Back 418

Sugars, glycols, alcohols, artificial sweetneers( saccharine,aspartame, sucralose-also activates bitter)

Front 419

Sweet taste
-T1R receptor family is immportant!
-Specifically T1R2 & T1R3 proteins make a dimer that is a _____
info

Back 419

That is a G-PROTEIN LINKED
- Broadly sensitive to sweet-tasting substances
-sweet receptors are NOT on the same cells as bitter and umami.

Front 420

Are sweet cells on the same cells as bitter and urami since all associated with TR??

Back 420

NO! Not ususally on the same cells

Front 421

Bitter taste- more than taste, also
a. stimuli
b. Protective taste
c. REceptors?

Back 421

-more than any other taste buds/receptor cells in mouth it is a PROTECTIVE TASTE.
a. Stumuli- usually orgain: K+ denatonium, caffeine, stychnine, quinine, nicotinie
b. Protective taste- highest # of receptors & lowest threshold for perception.. dont need many to taste bitter
c. Multiple receptors (50-80) in T2R family

Front 422

Salty taste
a. Stimuliated by:
b. Receptors:

Back 422

Salty taste
a. Stimuliated by: mostly by Na+ and somewhat by Cl-
b. Receptors:
1. ENaC (Na+ channel) & 2.Cl- via paracellular transport

Front 423

Urami taste- means?
a. Stimulus:
b. Receptor:
c. ex.

Back 423

Urami taste- Japanesse for delicious/salvioury
a. Stimulus: monosodium glutamate, enhanced by ribonucleotides
b. Receptor: T1R receptor family ( dimer of T1R1 & T1R3)
c. ex, cheese, wine, meats

Front 424

Taste perception:
5

Back 424

1.taste specficity-if high sweet/sour harder to differentatie what it is
2. Taste doesn't solely depend on combination of 5 receptors, also: fat, electric, metalic, pain, temp, smell, taste modifers=plant does this)
3. Taste adversion- not like what u use to
4. Taste adaptation- only occurs in 50% of receptors (rest of adapt more central) - & Threshold for sensitivity can change
5. Taste prefernce- gentetic, cultural influences

Front 425

You may weigh more if you are a nontaster bc?

Back 425

bc it takes more to get the taste of something than a supertaster.

Front 426

DO supertasters or nontasters have more somatosensory nerve endings?

Back 426

supertasters

Front 427

Transmission of Taste into CNS
1. Taste receptor cells synapse on ___order neurons
a. type of innervation
b. HOw do neurons enter CNS// nerves do?

Back 427

1. Taste receptor cells synapse on 1ST order neurons.
a. Redundant, bilateral innervaton.
b. Neurons enter CNS via CN 7,9,10
7=facial nerv-( from dif. taste papillae)e- Chorda Tympani Branch - ant. 2/3 of tongue (from extralingual)
-greater petrosal sf nerve- pap on saft palate- foiled fungiform.
9=Glossopharyngeal- post. 1/3 tongue- circumvelli
10-Vagus- pharynx, epiglottis, larynz- extralingual

Front 428

Transmission of taste into CNS.
1. Taste receptor cells synapse on 1st order neurons...
NOW
2. -4

Back 428

2. Second order neurons- cell bodies in the gustatory divsion of the nucleus of the solitary tract in the medulla (tractus solitarius)
3. Third order neurons: Cell bodies in the ventral posteromedial nucleus of the thalamus
4. Fourth order neurons: cell bodies in the gustatory cortex in the parietal lobe.

Front 429

What is CN1?
Are Olfactory receptors neurons or cells?

Back 429

CN1= Olfactory nerve
Olfactory receptor NEURONS

Front 430

Humans are able to differentiate 1000s of smells w/ relatively poorly ______

Back 430

poorly developed olfactory epithelium of only 10-20 million receptor cells.

Front 431

Olfactory Membrane
1. Location
2.Olfactory cells are primary:
a. receptors are located on
b. mylentated? large small?
c. Vm-
3. -3 types of cells

Back 431

Olfactory Membrane
1. Location- sup. portion of each nostril
2.Olfactory cells are primaryAFFERENT NEURONS
a. receptors are located on cilia that project into the mucus coating the nasal cavity
b. olfactory neurons are SMALL and UNMYELINATED
c. Vm- ~ -55mV
3. Sustentacular Cells, Basal Cells, Bowman's Gland
-Have cilia covered in mucus-surronded by sustentacular cells from bowmans gland

Front 432

Olfactory Receptor Proteins are on Cilia:
1. Most are what receptors?
what do they do?

Back 432

1. most are G-PROTEIN COUPLED Receptors (G-olf) coupled to adenylyl cyclase
a. Increased levels of cAMP open Na+ channels to depolarize the olfactory neuron
b. other recpetors may act via other 2nd messengers.

Front 433

Olfactory Receptor Proteins are on Cilia
1.Most are G-Protein coupled receptors (Golf) coupled to adenylyl cyclase.
2. To be perceived, Odorants must : 3 things

Back 433

2. To be perceived, odorants must:
a. Enter the nasal cavity
b. Be partially water-soluble ( to pass through mucus)
c.be partially lipid-soluble- bc way receptors are in cilla bc some blockages.. must attach to receptor

Front 434

Olfactory Receptor Proteins are on Cilia:
3.Adaptation
a. how much is achieved in how short of time?
b.longer term adapt

Back 434

3.Adaptation:
a. 50% of adapt. is achieve inthe first second
b. Further receptor adaptation is limited and slow

Front 435

Olfactory Receptor Proteins are on Cilia:
4. Termination of Smell Perception:
Odorants must diffuse away....

Back 435

4. Termination of Smell Perception:
Odorants must diffuse away, be BROKEN DOWN by ENZYMES, or ADAPTATION OCCURS.

Front 436

Olfactory Receptor Proteins are on Cilia:
5. Coding of Olfaction.
a. Olfactory receptor proteins are NOT
b. Different olfactory receptor proteins response to same odor?
c. patterm?

Back 436

5. Coding of Olfaction.
a. Olfactory receptor proteins are NOT Dedicated to single odorant-(a moderate activates it, but B really does and C slightly does, but could change for amother one)
b. Different olfactory receptor proteins respond DIFFERENTLY to same Odarants
c. Cross-fiber pattern code

Front 437

What is hypogeusia?

Back 437

diminished sense of taste

Front 438

What is hypergeusia?

Back 438

increased sense of taste

Front 439

What is dysgeusia?

Back 439

Taste is actually sour, but interpretted as sweet

Front 440

OraL malodours you may smell:
1. halitosis? associated with?

Back 440

Halitosis- voltatile sulpher compounds (VSCs produced by GRAM-negative anaerobic bacteria.
-alkaline saliva, decreased saliva, inflammation

Front 441

OraL malodours you may smell:
2. A few systemic diseases that alter breath- not in oral cavity..5ish groups

Back 441

1.TB, pneumonia, lung cancer, tonsilitits.
2. Hiatal hernias, gastroesophageal reflux, gastirc ulcer
3. Achalasia- sig. smell- sphincter sep stomach from esphogus- food builds up
4. Diabetic Ketoacidosis- sweet
5. Hepatic & renal failure

Front 442

Normal temp ranges- depends on:
Tongue:
mucosal surface of lips:
Facial skin temp:
Skin temp (hand, forearm, fingers):

Back 442

Normal temp ranges- depends on: body part... move outward=cooler
Tongue: 36-37C
mucosal surface of lips: 34-35C
Facial skin temp: 33-34C
Skin temp (hand, forearm, fingers):30-34C

Front 443

Does Cicadium rythm have to do with temp?

Back 443

coolest- am- 6:00am
warmest. evening

Front 444

Thermoreceptors are what type of receptors? and where found>

Back 444

-Free Nerve endings-
-Commonly found in: SKin, Hypothalamus, spinal cord, and deep tissue

Front 445

Temperature sensation and thermoreceptors
a. Cool and warm receptors innervate what?
b.More cool or warm receptors at any skin surface?
c.Extreme cold or heat activate?

Back 445

a. Cool and warm receptors innervate
b. There are 3-10 times as many COOL receptors at any skin surface
C. NOCICEPTORS- are activated by extreme cold or heat!

Front 446

How is the mechanism of thermal sensation most likely achieved?

Back 446

by sensing a change in metabolic rate

Front 447

The mech of thermalsensation is most likely achieved by sensing a change in metabolic rate.
A. Temp Increases the rate of
B. At least ____ ________ receptor potentials have been id in mice, each sensitive to a dif temp. range.
c. Some chemicals elicit-

Back 447

A. Temp Increases the rate of intracellular chem rxns > 2 times per 10C change.
B. At least 6 TRANSIENT receptor potentials have been id in mice, each sensitive to a dif temp. range.
c. Some chemicals elicit-THERMAL SENSATION

Front 448

Once thermoreceptors are activated:
a. Warm signals are transmitted by what type of fibers?
B. cold signals are transmitted by what type of fibers?

Back 448

a. Warm signals are transmitted by C and A-o fibers.. mostly C fibers
B. cold signals are transmitted by A-o and C fibers. MOSTLY A-o fibers tho!
Cool sensation perceived quicker than warm c fibers

Front 449

Temp perception is based on?

Back 449

The activation of a combination of receptors.

Front 450

If skin reaches freezing, cold/pain fibers

Back 450

are no longer stimulated

Front 451

What is Paradoxical cold?

Back 451

At 45C heat/pain fibers are activated, sometimes cold fibers are activated too

Front 452

a.Damage from & detection of hot pain is:
b.Damage & detection of cold pain is:

Back 452

a.Damage from & detection of hot pain is: ALMOST IMMEDIATE
b.Damage & detection of cold pain is: sLOWER ( ~10SEC)

Front 453

At what temp is there an equal activation of cool and warm receptors?

Back 453

34-35C... aver. skin temp.

Front 454

Hot and cold pain feel different, although both can result in:
Potentia ltissue damage- hot cold
Tissue damage- hot cole

Back 454

--Tissue damage!
Potential tissue damage:
Cold- <15C (59F)
Hot >45C(113F)
Tissue damage:
Cold- <0C(32F) Hot- >50C (122F)

Front 455

Cold pain:
-Hot pain:

Back 455

Cold Pain: Tickling, pricking, aching, burning, numbing
Hot Pain: Sharp, Pricking, Stinging, Burning , Throbbing

Front 456

Adaptation of Thermoreceptors- Most are what rate?

Back 456

Most are slow and wont completely adapt.

Front 457

Adaptation of thermoreceptors:
a. Rapidly & Slowly-adapting receptors- when?? how>
b. If temp reaches 1 of pain thresholds, what happens to the stimulus?

Back 457

a. Mostly (but never completely) adapt to constant temperature, THey QUICKLY change their activity in response to changes in temp./ can distinguish small change.
b. If temp reaches 1 of pain thresholds, THE SENSATION BECOMES MORE PERSISTENT THROUGH THE STIMULUS= MUCH MORE AWARE.

Front 458

Sensitivity of Thermoreceptors:
--> Warm and cool receptors are best able to dect a change where>??

Back 458

the mid-range of their temp sensitivity
warm- 25 C, & least likely at 10c or 35C

Front 459

Sensitivitiy of Thermoreceptors:
If nociceptor are simultaneously activated, the system is what??

Back 459

is better able to discern small changes in temp

Front 460

How is the perception increased by summation of thermorectptors?

Back 460

as temp Inc. (or decr.) w/in range of a thermorecptor's sensitivity, more and more receptors are activated, based o their varying thresholds. ( there is also an increase in the rate that thermal receptors fire ( but not nociceptors)

Front 461

Summation of thermoreceptor info:
The greater the area of skin affected by a stimulus...
ex. Pool- if stick toe in and ok, but jump in and freezing...

Back 461

The greater the # of receptors activated & thus the perveived sensation.
_ greater ability for dection of a temp. stimulus if a large region is activated

Front 462

Thermosensation in the oral cavity.
1. Receptors are 1' sentive to ____ but certain receptors are also sensitvie to chemicals.
a. Vanilloid receptor subtype-3 activations what does it do?
B. Cold-Menthol Receptor Type 1 (CMR1)- menthol compounds, fx

Back 462

1. receptors senstive to temp 1'
a. VRL1 Receptor (VR1) (spicy foods,etc).
--> Activated by: 1.capsaicin (perception of mean is warm, even tho it isnt) 2.temperature >43C, 3.Protons
--->FX:Decreases the threshold of channel activation so that the heat is perceived at 33C.
B. CMR1- Menthol & related compounds(tooth paste, gum assocatiated w/cool sensation).
--->FX- Decreases the threshold of the channels so that warmer compounds are perceived as cold.

Front 463

Characteristics of Thermoreceptors in Orofacial Region:
a. more cool or more warm receptors?
b. pts indicate can sense what?

Back 463

a.more cool than warm receptors
b. pts- better able to accurately detect ibcrements of waming rather than cooling- bc if start out in middle of warm--> better able to snese a change then towards end.

Front 464

Thermoreceptors in Orofacial Region:
C. Why are pts most senstive to the temp of drink/food when enters the mouth?

Back 464

Bc physical adaptation of it.. blow out - quickly changes - 20degrees w/in seconds.
- once in mouth, rapidly changes before thermoreceptors can work.

Front 465

Perception of and response to food temp:
1. The physical & textual properties of food influence temp perception.. ex??

Back 465

Fat- seems warmer bc insulator
water- seems colder even when same temp

Front 466

Perception of and response to food temp:
2. Movement of food in oral cavity---

Back 466

Drastically alters temp.

Front 467

Perception of and response to food temp:
3. Higher temp foods do what to temp perception?

Back 467

Higher temp foods increase the release of odor molecules and decrease food's viscosity... want it more!

Front 468

Perception of and response to food temp:
4. Direct warm or cool stimulation of the tongue can elicit what kind of taste?

Back 468

Warm- Sweet taste
Cool- Sour or salty taste

Front 469

Perception of and response to food temp:
Full dentures: Acrylic polymers vs. metal bases

Back 469

Acrylic polymers- less sensitive to temp bc insulator

Metal base- more senstive to temp= fiurther change in taste receptors

Front 470

What is nociception?? Wjat esxperience is it?? sensory or motor or emotional or other?

Back 470

Nociception- The perception of pain.
-The experience is sensory and emotional.

Front 471

Why do we sense pain? 3 things

Back 471

Sothat our body can dect, localize, and limit tissue damage

Front 472

All Nociception produces _____, but not all _____ results from Nociception.

Back 472

All Nociception produces PAIN but not all PAIN results from Nociception.

Front 473

Pain is never ____/.... regardless of the cause.. so it should be treated.

Back 473

Never BENIGN!!

Front 474

What is the most common/#1 reason patients seek healthcare?

Back 474

PAIN

Front 475

What TYPE of pain is good pain?

Back 475

Acute pain- physiological pain... this is short pain- bc it will be recovered from.. much easier to treat

Front 476

functional unit of cardiac and skeletal muscle?

Back 476

sacromere

Front 477

What is the importance of the dystrophin-glycoprotei complex?
1. importens of dystropin>
2. provides what?
3. muscualr what.

Back 477

1. Dystropin protein connects thin filaments glycoproteins in sarcolemma.. important, bc if not attach to sacromere, then it doesn't do anything.. no contraction... just wasted energy
2. Proveds scafflolding for sarcomeres
3. Muscluar dystrophies

Front 478

Why is titin important part of cytoskeletal proteins in a sacromere?

Back 478

Orients thick filaments in regard to thin filaments. Allignments

Front 479

What must happen in skeletal muscle fiber for a contraction to occur?

Back 479

increase in intracellular ca++

Front 480

What does topomyosin notmally do?

Back 480

Prevents a strong bond between the myosin head & G-Actin molecules

Front 481

How does myosin head bind to actin to have power stroke?

Back 481

By troponin binding to cytosolic Ca++ . it pulls the tropomysin away from the myosin binding site on actin

Front 482

In the contraction of skeltal muscles... where does most of the Ca++ come from?

Back 482

Sacroplasmic reticulum (SR)- which is just a modified ER that sequesters ca++

Front 483

What does nebulin do?

Back 483

Entire length of thin filament.. makes sure they are the same length

Front 484

What is the functional unit of cardiac and skeltal muscles?

Back 484

sacromere

Front 485

What determins the contraction of a skeletal muscle?

Back 485

# of sacromeres

Front 486

What do Alpha -actin do?

Back 486

Link thin filament to Z line

Front 487

Mysonin head is also converted to attached to actin by another way other than troponin/trpoomyosin...
enzyme, break down?

Back 487

Myosin also fx as an ATPase enzyme.. Breaks down ATP and changes the conformation of the head

Front 488

What do t-tubules do?

Back 488

They are invaginations of sarcolemma- t-tubles go inseide the cell, so more of the cell can reach AP

Front 489

As the AP in skeletal muscles trave down the membrane, down t-tubules, activates _____-_____ _____ receptors on the T-tubules. In turn these open _____ ____ (______ receptors) on the ____. Then what happens?

Back 489

As the AP in skeletal muscles trave down the membrane, down t-tubules, activates VOLTAGE-SENSITIVE DHP receptors on the T-tubules. In turn these open CA+ CHANNELS (RYANODINE receptors) on the SR. CA++ GOES FROM SR TO THE SARCOPLASM.

Front 490

In skeletal muscle, what insures the spread of AP (& Ca++) throughout the cell?

Back 490

Intracellular structure of myocytes

Front 491

Why do skeletal muscles fatigue? 6

Back 491

NOT DUE TO lack of ATP.
1. Hperoplarization of Vm- AP cuases K to move out=> more (-) charge in cell=> makes harder and harder to excite cell.
2. GLYCOGEN DEPLETION-most common
3. Reduction in blood flow (metabolite build-up)- harder to get blood in & harder to get metabolites out.
4. Decreased ACh- constant stimulation decreases ACh
5. Central Fatigue- other NT deplete&change pathway
6. Builds up due to lack of O2 ph rises

Front 492

Cross bridge clycling (sliding filament theory)
What must be present for this?

Back 492

BOTH Ca+ and ATP

Front 493

Cross bridge clycling (sliding filament theory)
What is the shortest state?

Back 493

Rigor state... ca present

Front 494

Cross bridge clycling (sliding filament theory) 5 steps

Back 494

1. Rigor State: Myosin & Actin are tightnly bound (Ca++ must already be present- shortest state)
2. ATP binds myosin, Decr. afffinity for actin & the 2 separate
3. Myosin head moves in the direction of the Z line, ATP is hydrolyzed (allows for change in myosin head)
4.Myosin binds the next actin (1 closer to Z line) & power stroke occurs (pulls actin toward the M line).
5.ADP is released and actin & myosin resume the brief rigor state.

Front 495

Relaxation of Skeletal Muscle
3 things must happen:

Back 495

1. Alpha motor neuron must stop firing (must get reat of ca++ to do this- done by caATPas)
2.Intracellular Ca++ concentrations must decrease
-->a.Ca++ ATPase on SR, -->b.Tropomyosin moves & covers actin's myosin binding site. -->c.Actin slowly slides back to its orginal resting place & the sacormere returns to its orginal length.
** for relaxtion to occur , Ca must be removed, but ATP must be present, other wise- rigor state maintained.
Need

Front 496

What must be removed or not removed for relaxation of skeltal muscles?

Back 496

CA- removed
ATP must be present- other wise rigor state maintained
NEed ATP for both relax & contract.
relax- bc it removes ca and dissociates actin from myosin

Front 497

What are the 3 types of skeletal muscle fibers?

Back 497

1. Slowtwitch- type1- dont fatigue very rapidly
2. Fast Twitch- Oxidative- Typle 2A- more myoglobin-red color
3. Fast twitch- 2B- whitemeat- strongest

Front 498

3 types of skeletal muscle fibers:
1. Slow twitch- Type 1 muscle fibers
Color:
Myosin Atpase Activity:
SR Ca++ Atpase :
Diameter:
Glycotic Capacity:
Oxidative capacity:
Fatigue:

Back 498

1. Slow twitch- Type 1 muscle fibers
Color: Red
Myosin Atpase Activity: Slow
SR Ca++ Atpase :Moderate
Diameter:small
Glycotic Capacity: moderate
Oxidative capacity:High
Fatigue: Slow

Front 499

3 types of skeletal muscle fibers
2. Fast-Twitch- type 2A- Oxidative Glycotic
Color:
Myosin Atpase Activity:
SR Ca++ Atpase :
Diameter:
Glycotic Capacity:
Oxidative capacity:
Fatigue:

Back 499

2. Fast-Twitch- type 2A- Oxidative Glycotic
Color: Red
Myosin Atpase Activity: Fast
SR Ca++ Atpase : Fast
Diameter: Moderate
Glycotic Capacity: High
Oxidative capacity:Moderate
Fatigue:Fast resistnat

Front 500

3 types of skeletal muscle fibers:
3.Fast twitch- type 2B- Glycolytic
Color:
Myosin Atpase Activity:
SR Ca++ Atpase :
Diameter:
Glycotic Capacity:
Oxidative capacity:
Fatigue:

Back 500

3.Fast twitch- type 2B- Glycolytic
Color:White
Myosin Atpase Activity: Fast
SR Ca++ Atpase :Fast
Diameter:Large
Glycotic Capacity:High
Oxidative capacity:Low
Fatigue:Fast Fatigable

Front 501

3 types of skeletal muscle fibers:
diamter relates to strength?
bigger =

Back 501

Bigger the diameter the more powerful it is

Front 502

What is Sarcopenia?

Back 502

type of decrease in m. fiber. In association with dz state.

Front 503

Hyperplasia is?

Back 503

Have more m. fibers very rare to see spliting of m. fibers to increase #

Front 504

Can skeletal muscle fiber types change from one type to another?

Back 504

Type 1 to 2 cannot happen, but from from type 2a to type2b can happen

Front 505

What is a motor unit?

Back 505

A motor unit is the alpha motor neuron & the muscle fiber it innervates

Front 506

Motor units are recruited in order of the SIZE
Small motor units?

Back 506

Small motor units- recruited first.
-Smallest motor units control fewer fibers

Front 507

What does the increase in # of motor units activated do?

Back 507

increases the total tension produced by contraction of muscle

Front 508

What is asynchronous recruitment?

Back 508

Active type 1 first then type 2a, type 2b. IF more m. fibers are firining then have more contraction.

Front 509

What determines the TYPE of skeletal muscle contraction?

Back 509

1. amount of load
2. force generated

Front 510

Force produced is great enough to move a load?

Back 510

isotonic contraction

Front 511

Force produced is less than the load= no movement... every contraction starts out this way.

Back 511

Isometric contraction

Front 512

Contraction of whole skeletal muscle is graded.. so to increase the # of muscle fiber contracting, must

Back 512

Increase total force by increasing the frequency of fiber activation??

Front 513

For a single muscle twicth ( 1 muscle fiber) the tension developed is altered by:

Back 513

sacromer length= optimal length

Front 514

Velocity of contraction ( distance moved/time) depends on what?
Ex. Why would one have a lower/slowed down contraction?

Back 514

Depends on the load a fiber is contracting against.
ex- Speed of contraction lowers/slows down if load is heavier

Front 515

What are the 2 sensory units of skeletal muscle reflexes?

Back 515

1. Muscle spindles
2. golgi tendon organ (located in tnedon & not m. proper)

Front 516

What is are extrafusal fibers?

Back 516

Skeletal muscle ALPHA Motor Neuron. Efferent neuron that releases ACh & causes contraction of the extrafusla fiber (skel. m.)

Front 517

What is a muscle spindle?
& what does it contain?

Back 517

Small structure w/in the extrafusal fiber that contains:
1.Intrafusal fibers -contacticle elements
2.Sensory receptors- Mechanosensitive receptors that monitor changes in muscle length.

Front 518

What is a Gamma motor neuron?

Back 518

Efferent neuron that causes contraction of intrafusal fibers

Front 519

What is the stimulus for the muscle spindle reflex?

Back 519

Stretch.
When muscle strectches the sensory fibers of the muscle spindle are squeezed.
Afferent info enters the spincal cord & activates both alpha and gamma motor neurons.

Front 520

When activating the alpha motor neuron in regaurd to strtecthing a muscle spindle.. what does it stimulate?

Back 520

This stimulates muscle (extrafusal fiber) contraction

Front 521

When activating the gamma motor neuron in regaurd to strtecthing a muscle spindle.. what does it stimulate?

Back 521

This stimulates intrafusal fiber contraction. IF intrafusal finers did not contract, the sensory fibers would not be able to sense a further change in muscle length since they would be slack.

Front 522

Muscle spindles are sensitive to what?

Back 522

Muscle length

Front 523

Waht is the effect of muscle spindle activation?

Back 523

The effect of Muscle Spindle Activation is CONTRACTION.
- The reflex has dynamic (immediate) & static (maintains tone-constant contraction) reflex components.

Front 524

Alpha-gamma coactivation is Nescessary bc it allows what ?? (muscle spindle).

Back 524

This allows the muscle spindle to maintain sensitivityto changes in muscle length.

Front 525

The route of Alpha and gamma coactivation... Starting with 1. muscle stretches.

Back 525

2. Increase in firing of sensory nerve
3. Sensory nerve activates alpha & gamma motor neurons.
4. Extrafusual & intrafusal fibers contract
5.Sensory nerve retains sensitivity to muscle length.
Anytime the Alp-motor neuron is activated, the gamma motor neuron is also activated.

Front 526

What is the Golgi Tendon Organ (GTO) Reflex?

Back 526

-Inhibitory stretch reflex
-Protective reflex

Front 527

Golgi tendon organs are?

Back 527

-Mechanosensitive receptors found at the junction of tendons and muscle. Sensitive to change in force.

Front 528

What is the stimulus for GTO reflex?

Back 528

Tendon Stretch
1. Tendon stretch in response to contraction ( particularly isometric)
2. Etreme stretch of the tendon will squeeze the GTO & afferent neurons will send info into spinal cord.-->stimulates an inhib. interneuron, which decreases the activity of the alpha motor neuron...-->Skeletal muscle contraction is decreased (relaxation.)

Front 529

The effect of GTO Reflex is:

Back 529

The effect of GTO is Decreased Contraction. This reflex also has dynamic & static componenets.

Front 530

Muscle Tendon Reflex( stretch REflex) review: receptors, sensitive, activation

Back 530

-Receptors are muscle spindles
-Sensitive to change in muscle length
-When activated- Contract muscle

Front 531

GTO Reflex review
-Receptors? Senstive? activated?

Back 531

- Receptors are GTO
-Sensitive to change in Tension
-When activated- Relax the muscle