• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/83

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

83 Cards in this Set

  • Front
  • Back
Conduction Velocity
V= λ/T
Velocity = Length constant/Time constant
Length constant
λ = square root of (Rm/Ri)

Length constante equals the square root of Membrane resistance over Internal resistance

membrane resistance is inversely related to speed current flows across membrane (how far depolarizing current will spread along a fiber

Internal resistance is inverseley proportional to the ease current passes thru cytoplasm and inversely proportional to the cross sectional area of the fiber
Time constant
T = Rm Cm

Time constant = Membrane resistance times membrane capacitance

Time constant refers to the amount of time it takes reach 63% of its final value (100% would be the total change from RMP to threshold)

Membrane capacitance is the ability of the cell membrane to store a charge
contiguous conduction
AP spreads across every portion of membrane because it is an unmyelinated fiber
Saltatory conduction
Generates APs 50 times faster than unmyelnated fibers of comparable size

myelination via schwann cells in PNS & oligodendrocytes in PNS
Multiple sclerosis
most common demyelinating disease of the CNS

(oligodendrycytes)
Hyponatremia
-Plasma Na levels below normal

-Reduces concentration gradient and driving force for Na

-causes decrease in magnitude of overshoot & rate of rise of upstroke
Hyperkalemia
-Plasma K levels below normal

-Depolarizes RMP

-continuous depolarization innactivates some of the VG-Na channels

-because fewer Na channels are available to initiate APs a greater stimulus will be needed
Hyperparathyroidism
If plasma concentration of phosphate decreases there will be an increase in free Ca to reduce neuron excitability
Hypoparathyroidism
If plasma concentration of phosphate increaes ther will be a decrease in free Ca to increase neuron excitability
effect of free ionized Ca on neuron excitability
greater Free Ca stabalizes plasma membrane and makes it less excitable

less free Ca makes threshold potential more negative and neuron becomes more excitable
background channels
These channels spontaneously open in the absence of an external stimulus.

They are generally largely responsible for generating the resting membrane potential.
Hyponatremia
-Plasma Na levels below normal

-Reduces concentration gradient and driving force for Na

-causes decrease in magnitude of overshoot & rate of rise of upstroke
Mechanosensitive channels
These channels, also known as stretch-activated channels, respond to membrane deformation, pressure of touch, and also other sensory inputs (e.g. sound, blood pressure, temperature).

Stimulating mechanosensitive channels generates graded potentials.
Hyperkalemia
-Plasma K levels below normal

-Depolarizes RMP

-continuous depolarization innactivates some of the VG-Na channels

-because fewer Na channels are available to initiate APs a greater stimulus will be needed
Ligand-gated channels
Also known as chemically-gated channels, these channels respond to chemical signals.

Opening ligand-gated channels generates graded potentials.
Hyperparathyroidism
If plasma concentration of phosphate decreases there will be an increase in free Ca to reduce neuron excitability
Voltage-Gated Channels
these channels have a voltage sensor that alters the channel conformation when membrane potential changes over a specific range.

opening of voltage-gated ion channels initiate action potentials, not graded potentials.
Hypoparathyroidism
If plasma concentration of phosphate increaes ther will be a decrease in free Ca to increase neuron excitability
Examples of graded potentials:
Postsynaptic potentials
End-plate potentials
Pacemaker potentials
Slow-wave potentials
effect of free ionized Ca on neuron excitability
greater Free Ca stabalizes plasma membrane and makes it less excitable

less free Ca makes threshold potential more negative and neuron becomes more excitable
background channels
These channels spontaneously open in the absence of an external stimulus.

They are generally largely responsible for generating the resting membrane potential.
Mechanosensitive channels
These channels, also known as stretch-activated channels, respond to membrane deformation, pressure of touch, and also other sensory inputs (e.g. sound, blood pressure, temperature).

Stimulating mechanosensitive channels generates graded potentials.
Ligand-gated channels
Also known as chemically-gated channels, these channels respond to chemical signals.

Opening ligand-gated channels generates graded potentials.
Voltage-Gated Channels
these channels have a voltage sensor that alters the channel conformation when membrane potential changes over a specific range.

opening of voltage-gated ion channels initiate action potentials, not graded potentials.
Examples of graded potentials:
Postsynaptic potentials
End-plate potentials
Pacemaker potentials
Slow-wave potentials
Temporal summation
summation of several ESPS occurring very close together in time by successive firing of a single presynaptic neuron
Spatial summation
summation of several ESPS ocurring simultaneously from several different presynaptic imputs
Generation of Action Potentials: Summary
Step 1: Resting State
Voltage-gated Na+ and K+ channels are closed

Leakage accounts for all movement of Na+ and K+
Generation of Action Potentials: Summary
Step 2: Depolarization
At threshold ALL voltage-gated channel gates (both Na+ and
K+) are triggered or activated


Activation gates of voltage-gated Na+ channels open quickly


More voltage-gated Na+ channels open by positive feedback mechanism


Na+ ions rush into cytoplasm causing rapid depolarization

Inner membrane changes from negative to positive
Generation of Action Potentials: Summary
Step 3: Repolarization
At peak (+30 mV) Na+ inactivation gates close (Na+ channel inactivation) and K+ channels open.


Na+ channels begin to reset to resting conformation when membrane reaches normal resting potential (-70 mV).


K+ channels begin to close (delayed closing) when membrane reaches normal resting potential (-70 mV).
Generation of Action Potentials: Summary
Step 4: Hyperpolarization
K+ channels finish closing after membrane is hyperpolarized to -80mV and returns back to resting; while almost all Na+ channels are reset to resting conformation.
Absolute refractory period
Interval during which NO stimulus can elicit an
action potential.

Most voltage-gated Na+ channels are inactivated.
Relative refractory period
Interval when a SUPRANORMAL stimulus is
required to elicit an action potential.


Due to elevated gK coupled with the residual inactivation of voltage-gated Na+ channels.
Negative feedback system
-Primary type of homeostatic control
-Maintains stability by defending set points
-Opposes initial change
-Compnents:

Sensor- Monitors magnitude of a control variable

Integrator- (Control center) Compares sensor's input with a set point

Effector- Makes a response to produce a desire effect

e.g. thermastat
Positive feedback system
-Do not occur as often as negative feedback system
-Drives physiological values away from set point; destabilizing
-Amplifies initial change

e.g. Uterine contractions become increasingly stronger until birth of baby due to positive feed back increasing oxytocin secretion

positive feedback cycle for opening of Na+ gated channels
Homeostasis
Redundancy:
Hierarchy and Competition:
Adaptability:
Redundancy: The more vital the parameter is, the more systems the body mobilizes to regulate it.

Hierarchy and Competition: Feedback loops may have opposite effects. The body places a priority ranking among feedback loops.

Adaptability: Flexibility of feedback loops allows for many forms of physiological adaptation or acclimatization (e.g. response to altitude).
Integral Proteins
Proteins that are embedded in, and anchored to, the cell membrane
Peripheral proteins
Proteins that are loosely attached (not embedded) to either the intracellular or the
extracellular side of the cell membrane
Functions of membrane proteins
Channels
Transporters or carriers
Pumps
Receptors
Adhesion molecules (CAMs)
Ability to recognize "self"
aquaporins
proteins formed channels specific for passage of water

allow flow of 1 million water molecules per second
Fick's law
Simple diffusion

a steady state balance will occur with equal concentrations and volumes on each side
osmotic pressure
results from the difference in water concentration

Can be estimated from Van't Hoff equation
Hydrostaic pressure
results from gravitational force on a column of fluid

Since plasma membranes deform easily, the hydrostatic pressure difference is usually zero and does not provide a significant driving force for water transport
Van't Hoff equation
Used to determine osmotic pressure

Osmotic pressure = g C @ RT

g= # of particles per mole

C= concentration (mmol/L)

@= reflection coeffiecient (varies from 0-1)

R= Gas constant (0.082L-atm/mol-K)

T= absolute temp (K)
Isoosmolar

Hyperosmolar

Hypoosmolar

effective osmolarity
having the same osmolarity as normal extracellular fluid (approximately 290 mOsm); includes both permeant and impermeant particles

having a greater osmolarity than normal extracellular fluid

Refers to the osmolarity of non-permeable particles in solution

having a lower osmolarity than normal extracellular fluid
Response to Cell Swelling
Most commonly the Cl-and K+ channels are activated

Resultant net efflux of Cl-and K+ decreases osmolarity and water diffuses out of the cell

Cell volume is restore to normal
Response to Cell Shrinkage
Cell shrinking activates solute uptake mechanism

Most commonly the Na+/H+ exchanger is activated (Na+ in /H+ out)

H+ extrusion alkalinizes the cell and activates the Cl-/HCO3- exchanger

Resultant net increase in intracellular Na+ and Cl- draws water into the cell

Cell volume is restored to normal
Flux:
Efflux:
Influx:
Net Flux:
Flux = Rate of diffusion

Eflux= diffusion out of cell

Influx= diffusion into cell

Net flux = difference between influx and eflux
Carrier-mediated transpo
Accomplished by membrane carrier flipping its shape

Can be passive or active
The Na+-K+ ATPase (Na+-K+ pump)
Electrogenic (imparts an electrical imbalance between the ECF and ICF)

Maintains gradients of Na+ and K+

pumps 3 Na+ out and 2 K+ in

Utilizes ATP

Inhibited by:
-cardiac glycosides
-ouabain
-inhibit the Na+-K+ ATPase by binding to the E2~P conformation form near the K+-binding site on the extracellular side, thereby preventing the conversion of E2~P back to E1. By disrupting the cycle of phosphorylation-dephosphorylation, these drugs disrupt the entire enzyme cycle and its transport functions.
2 types of 2ndry Active transport
Cotransport: occurs when uphill solute moves in same direction as Na+

Countertransport: occurse when uphill solute moves in the opposite direction of Na+
Total Body Water
TBW = ICF + ECF

ICF = 2/3 of TBW

ECF = 1/3 of TBW
Interstitial fluid (3/4 ECF)
Plasma (1/4 ECF)

Water accounts for 50-70% of body weight
TBW=.7LBM + .1AT
Body Water Compartments: Daily Intake/Daily losses
Ingested: liquids or foods = 2100 ml/day

Produced from the oxidation of carbohydrates
= 200 ml/day

Loss that is not precisely regulated
and not aware of
-Evaporation from lungs: 350 ml/day
-Diffusion through skin: 350 ml/day

Fluid loss in sweat = 100 ml/day

H2O loss in feces = 100 ml/day

H2O loss by kidney as formation of urine = 1400 ml/day
Plasma osmolarity
Plasma Osmolarity = 2Na + Glucose/18 + BUN/2.8

At equilibrium all compartments have the same osmolarity; estimated from plasma osmolarity
Gain of Isotonic Fluid:
Isosmotic volume expansion

what effect would this have?
IncreaseinECFvolume

No change in ICF volume

IncreaseinTBW

No change in ECF or ICF osmolarity

No shift in H2O between ICF and ECF

Decrease plasma protein concentration and hematocrit (diluted because of increase in ECF volume)

e.g. salin infusion
Loss of Isotonic Fluid:
Isosmotic volume contraction

what effect would this have?
Decrease in ECF volume

No change in ICF volume

Decrease on TBW

No change in ECF or ICF osmolarity

No shift in H2O between ICF and ECF

Increaseplasmaproteinconcentrationand hematocrit (concentrated because of loss in ECF volume)

e.g. diarrhea
Gain of Hypotonic Solution:
Hypoosmotic volume expansion

what effect would this have?
Increase in ECF volume

Decrease in ECF osmolarity

Shift in H2O from ECF to ICF

Increase in ICF volume

Decrease in ICF osmolarity

Increase in TBW

Decrease plasma protein concentration (by dilution)

No change in hematocrit (no net change):
-RBC volume increases because of water shift into RBCs, but concentration of RBCs decreases by dilution.

e.g. drinking pure water, syndrome of inappropriate antidiuretic hormone secretion SIADH
Gain of Sodium

what effect on water balance would this have?
Increase in ECF osmolarity

Shift in H2O from ICF to ECF

Decrease in ICF volume

Increase in ECF volume

Increase in ICF osmolarity

No change in TBW

Decrease plasma protein concentration (by dilution)

Decrease hematocrit
-RBC concentration decreased by dilution and also because
of water shift out of RBCs decreasing cell volume.

e.g. high salt intake
Loss of sodium

what effect on water balance would this have?
Decrease in osmolarity

Shift in H2O from ECF to ICF

Increase in ICF volume

Decrease in ECF volume

Decrease in ICF osmolarity

No change in TBW

Increase plasma protein concentration (by fluid loss)

Increase hematocrit
-RBC concentration increased by ECF fluid loss and also because of shift of H2O into RBCs, increasing cell volume.

e.g. aldosterone insuficiency (aldosterone promotes Na reabsorbtion & prevents loss in urine)
Loss of Hypotonic Solution:
Hyperosmotic volume contraction

what effect would this have
Decrease in ECF volume

Increase in ECF osmolarity

Shift in H2O from ICF to ECF

Decrease in ICF volume

Increase in ICF osmolarity

Decrease in TBW

Increased plasma protein concentration (by fluid loss)

No change in hematocrit (no net change):
-RBC volume decreases because of water shift out of RBCs

e.g water depravation, sweating
but concentration of RBCs increases with fluid loss.
Isotonic Glucose Infusion

effect on water balance?
Increase in ECF volume with no initial changes in osmolarity (isotonic solution)

Glucose is metabolized into CO2 and H2O

Increase in ICF volume

Decrease in ICF osmolarity

Shift in H2O from ICF to ECF

Further increase in ECF volume (addition of hypotonic solution, e.g. water)

Decrease in ECF osmolarity

Increase in TBW

Decrease plasma protein concentration and
hematocrit (by dilution due to increase in ECF volume)
Magnitude of Membrane Potential
The magnitude of the potential depends on the number of opposite charges separated.

The greater the number of charges separated the greater the potential.
Driving forces for Diffusion of Ions through an Open Channel
Chemical driving force = concentration gradient

Electrical driving force = electrical gradient (negative ions attract positive ions)

Electrochemical gradient = the 2 combined to act in the same or opposite directions
Diffusion Potential:
-definition
-4 types
potential difference generated across the membrane when there is an unequal diffusion of positive and negative ions.

Equilibrium potential
-Chemical & electrical forces are equal & opposite


Resting membrane potential
-difference that exists across the membrane of excitable cells at steady-state. (-70mV)

Graded potential

Action potential
Typical Values for Equilibrium Potential for Common Ions
E Na+ = +65 mV

EK+ =-90mV

ECl- =-50mV

E Ca2+ = +120 mV
The Nernst Equation
Used to colculate equilibrium potential for an ion at a given concentration across the membrane

Eion = (60/z) log ( [ion]out / [ion]in)

E ion = equilibrium potential for ion (mV)

z = ionic valence of ion (charge +/-)

[ion]out = extracellular concentration for ion (mmol/L)

[ion]in = intracellular concentration for ion (mmol/L)
Ionic Ohm's Law
(chord conductance equation)

and Resting Membrane potential equation
Estimates membrane potential knowing equilibrium potentials and conductances for each ionic species in question

The ion with the higher conductance will have a greater effect on RMP

Since the resting membrane potential is determined almost entirely by Na+ and K+ concentrations and permeabilities, we can simplify the equation to include the equilibrium potentials and the relative conductance of Na+ and K+ only.

Em = (gK EK + gNa ENa) \ (gK + gNa)
Conductance (g)
Conductance = permeability

g = NPoY

where N = the number of channels

Po = the probability that a channel is open

Y = The conductance of a single open channel
The process of chemical transmission can be summarized by the following series of 7 steps:
Step 1: Neurotransmitter molecules are packaged into synaptic vesicles. Specific transport proteins in the vesicle membrane use the energy of an H+ gradient to energize uptake of the neurotransmitter in the vesicle.

Step 2: An action potential, which involves voltage-gated Na+ and K+ channels, arrives at the presynaptic nerve terminal.

Step 3: Depolarization opens voltage-gated Ca2+ channels, which allows Ca2+ to enter the presynaptic terminal.

Step 4: The increase in intracellular Ca2+ concentration ([Ca2+]i) triggers the fusion of synaptic vesicles with the presynaptic membrane. As a result, packets (quanta) of transmitter molecules are released into the synaptic cleft.

Step 5: The transmitter molecules diffuse across the synaptic cleft and bind to specific receptors on the membrane of the postsynaptic cell.

Step 6: The binding of transmitter activates the receptor, which in turn activates the postsynaptic cell.

Step 7: The process is terminated by (1) enzymatic destruction of the transmitter (e.g., hydrolysis of ACh by acetylcholinesterase), (2) uptake of transmitter into the presynaptic nerve terminal or into other cells by Na+- dependent transport systems, or (3) diffusion of the transmitter molecules
away from the synapse.
10 Common Neurotransmitters
Acetylcholine
-Neuromuscular junction

Glutamate
-Major excitatory in CNS

Glycine
-Ihibitory NT

Norepinephrine
Epinephrine
Dopamine
-Tyrosine derivatives

Serotonin

Histamine

y-Aminobutyric acid (GABA)

Nitric Oxide (NO)
-Gas; Inhibitory in CNS
Neuropeptides
Large molecules consisting of anywhere from 2 to 40 aa.

Synthesized in neuronal cell body and are subsequently moved by axonal transport to the axon terminal.

Packaged in large, dense-core vesicles present in axon terminal.

Dense-core vesicles undergo Ca2+ - induced exocytosis and release neuropeptides at the same time as neurotransmitters are release from synaptic vesicles.

Exhibit a slow, prolonged response by acting on adjacent neurons at lower concentrations than neurotransmitters.

Act as neuromodulators = chemical messengers that do not cause the formation of EPSPs or IPSPs, but rather bring subtle long-term changes that modulate (depress or enhance) the action of the synapse.
Model of synaptic vesicle fusion and exocytosis: 6 steps
Initial state
-Vesicles with synaptotagmin & syanptobrevin (a v-SNARE) move to the nerve terminal membrane which contains syntaxin & SNAP-25 (both t-SNAREs)

Formation of Ternary Complex of SNAREs
- n-sec-1 dissociates from syntaxin, allowing the syntaxin & SNAP-25 to form a complex. The distal end of synaptobrevin begins to wind around the syntaxin/SNAP-25 complex forming a ternary complex

Tightening of ternary SNARE complex
-the 3 SNAREs, synaptobrevin, syntaxin, & SNAP-25, continue to form a tight bundle of alpha helices, drawing vesicle & presnyaptic membranes into close apposition

Fusion & Exocytosis
-The entry of Ca and its binding to synaptotagmin triggers fusion

Disassembly of ternary SNARE complex
-alpha-SNAP and the ATPase NSF bind to the ternary SNARE complex and use the energy of ATP hydrolysis to disassemble the SNAREs

Recycling of SNAREs
-With the endocytosis of the vesicle, the syaptobrevin is effectively recycled. The syntaxin & SNAP-25 are now free for an additional cycle of vesicle fusion

3.
Neurotransmitters Can Activate Ionotropic or Metabotropic Receptors
Activation of an ionotropic receptor causes rapid opening of ion channels. This channel activation in turn results in depolarization or hyperpolarization of the postsynaptic membrane, the choice depending on the ionic selectivity of the conductance change

Activation of a metabotropic G protein-linked receptor results in the ␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣ cellular responses by direct interaction with either ion channel proteins or other second-messenger effector proteins.
Presynaptic Facilitation/Inhibition
Axoaxon?

An excitatory/inhibitory neuron synapse impinging on presynaptic terminal or axon can increase/decrease the amount of NT released from the presynaptic terminal.

-only one or the other, one nerve cannot do both
DRUG action: Blocks Ach release from presynaptic terminals

Effect?
Effect: total blockade, paralysis of respiratory muscles & death
Drug action: Competes with Ach for receptors on motor end plate

Effect?
Effect: Decreases size of EPP; in maximal doses produces paralysis of respiratory muscles and death
Drug action: AchE inhibitor

Effect?
Effect: Prolongs & enhances action of Ach at motor end plate
Drug action: Blocks reuptake of choline into presynaptic terminal

Effect?
Effect: Depletes Ach stores from presynaptic terminal
Clinical Applications:
Lambert Eaton syndrome
Autoimmune disorder caused by antibodies attacking the presynaptic voltage-gated Ca channels

Most often seen in patients with certain types of cancer such as small cell lung carcinoma
3 Exceptions to general rule of dual reciprocal innervation by the two branches of autonomic nervous system
Most arterioles and veins receive only sympathetic nerve fibers (arteries and capillaries are not innervated)

Most sweat glands are innervated only by sympathetic nerves

Salivary glands are innervated by both ANS divisions but activity is not antagonistic both stimulate salivary secretion
3 Regions of CNS Involved in Control of Autonomic Activities
Hypothalamus plays important role in integrating autonomic, somatic, and endocrine responses that automatically accompany various emotional and behavioral states

Medulla within brain stem is region directly responsible for autonomic output

Some autonomic reflexes, such as urination,
defecation, and erection, are integrated at spinal cord
Autonomic Agonists and Antagonists
Agonists
-Bind to same receptor as neurotransmitter
-Elicit an effect that mimics that of neurotransmitter

Antagonists
-Bind with receptor
-Block NT's response