Phgy 209

Front 1

Homeostasis

Back 1

-state of dynamic constancy

-at all levels of organization

-functional activities directed at maintaining "Milieu Interieur"

-failure to maintain disrupts normal function

Front 2

Homeostatically Controlled Factors

Back 2

-concentration of nutrient molecules

-concentration of O2/CO2

-concentration of waste

-concentration of electrolytes

-pH

-temperature

-volume/pressure

Front 3

Water

Back 3

-most abundant single constituent in body (45-75%)

-universal solvent where metabolic reactions take place

Front 4

Body Water %

Back 4

-skin: 70%

-muscle: 75%

-heart, liver, brain, kidney: 70-80%

-bone: 25%

-fat (adipose tissue): 10%

^main factor in determining variation in water content between individuals

-body water % varies with age, gender, weight

-body water remains in dynamic steady state (healthy)

Front 5

Water Balance

Back 5

INTAKE:
-oral fluid (~1.2L)

-oral intake as food (~1.1L)

-oxidative water from metabolism (~0.4L)

total = ~2.7L

OUTPUT:

-lungs (~0.4L)

-skin (~0.5L)

-kidneys (~0.5-1.2L)

-stool (~0.1L)

total = ~2.7L

Front 6

Obligatory Losses

Back 6

~1.5L of water/day

-insensible: ~1.0L

-urine + stool: ~0.5L

Front 7

Facultative Losses

Back 7

-vary with intake

-urine (kidney is major homeostatic organ)

Front 8

Insensible Perspiration

Back 8

1. Pure water

2. Passive evaporation (ambient temp/relative humidity)

3. Entire skin surface (present even in those lacking sweat glands)

4. Cotinuous

Front 9

Sweating

Back 9

1. Electrolyte solution

2. Active secretion

3. Sweat glands

4. Activated by heavy work/high temp

Front 10

Water Turnover

Back 10

~3-4% in adults

-in infants: much higher % of their total body weight

-body water helps maintaining normal solute concentrations

-helps maintain normal blood volume/pressure

Front 11

Reasons for Negative Water Balance

Back 11

1. Reduced intake

2. Excessive loss from gut (ex. vomiting)

3. Excessive sweating

4. Excessive loss in expired air (ex. dry air/high altitudes)

5. Excessive loss in urine

Front 12

Reasons for Water "Intoxication"

Back 12

1. Excessive intake

2. Renal system failure

Front 13

Intracellular Body Fluid

Back 13

-2/3 body fluids are intracellular

-make up 40% of body mass (~28L)

-high in K+/Mg2+, low in Na+/Cl-

Front 14

Extracellular Body Fluid

Back 14

-make up 20% of body mass (~14L)

-low in K+/Mg2+, high in Na+/Cl-

Major:

-plasma

-interstitial fluid

Minor:

-lymph

-transcellular fluid

Front 15

Plasma

Back 15

-fluid media in which white blood cells are suspended

~5% of ECF

Front 16

Hematocrit (Ht)

Back 16

-% of blood volume occupied by RBCs

= height of erythrocyte column/height of whole blood column

~45%

Front 17

Interstitial Fluid (ISF)

Back 17

-fluid which percolates between individual cells

~15% of ECF

Front 18

Lymphatic System

Back 18

-network of blind ended terminal tubules that coalesce to form larger lymphatic vessels

-merge to form ducts

-drain into large veins in chest

~1.2% of ECF

Front 19

Transcellular Fluid

Back 19

-aggregate of small fluid volumes

-secreted by specific cells into various cavities

-ex. intraocular, cerebro-spinal, synoidal, etc

<1.2% of ECF

Front 20

Indicator Dilution

Back 20

-measuring body fluids

Need to Know:

-total quantity of test substance

-concentration of substance/units of volume after dispersion

Procedure:

1. Introduce quantity (Q) of indicator into vein

2. Allow equilibrium

3. Remove volume of blood (V) and centrifuge

4. Measure concentration (C) in unit volume of plasma

Front 21

Indicator Choice for Indicator Dilution

Back 21

-non-toxic

-diffuses readily

-even distribution

-induces no changes in water distribution

-easy to measure

-ex. antipyrne, D2O, T2O

Front 22

Plasma Measurements

Back 22

-indicator must be restricted within blood

-unable to cross capillary wall

Front 23

Cell Membrane

Back 23

-phospholipid bilayer

-supports distinct compositions of ICF and ISF

-selectively permeable:

-highly permeable to H2O, lipid-soluble substances, dissolved gases, small uncharged molecules

-less permeable to large molecules, charged particles

Front 24

Bimolecular Phospholipid Bilayer

Back 24

-fluid-mosaic model:

-polar heads (hydrophilic)

-non polar tails (hydrophobic)

-polar region faces outwards, non polar inwards to cytoplasm/extracellular fluid

-cholesterol inserted to provide stability/rigidity

-differently charged ends (antipathic) help maintain fluidity

-integral/peripheral proteins

-glycocalyx

Front 25

Peripheral Proteins (Plasma Membrane)

Back 25

-loosely associated with phospholipid bilayer

-mostly on cytoplasmic side

Front 26

Integral Proteins (Plasma Membrane)

Back 26

-closely associated with phospholipids

-mostly antipathic

Front 27

Glycocalyx

Back 27

-comprised of carbohydrates and glycoproteins on outer side of plasma membrane

Front 28

Functions of Membrane Proteins

Back 28

-ion channels and transporters

-catalyze membrane reactions

-serve as receptors for receiving/transducing chemical signals from cell

-cell surface identity markers

-cell-cell adhesion

-attachment to cytoskeleton

Front 29

Passive Transport

Back 29

-diffusion

-carrier-mediated facilitated diffusion

-osmosis

Front 30

Active Transport

Back 30

-energy dependent

-carrier-mediated active transport (primary/secondary)

-pinocytosis

-phagocytosis

Front 31

Diffusion

Back 31

-movement of solute particles from region of high concentration to low

Front 32

Fick's Law of Diffusion

Back 32

J = PA (Co - Ci)

J = net flux

P = permeability coefficient

A = surface area of membrane

Co - Ci = concentration gradient

Front 33

Ion Channels

Back 33

-transport particles through plasma membrane

-may consist of a single protein or cluster of proteins

-show selectivity based on their diameter as well as the distribution of charges lining the channel

Front 34

Electrochemical gradient

Back 34

-simultaneous existence of electrical and concentration gradient for particular ion

-affects movement of ions

Front 35

Ligand-gated channels

Back 35

-open when molecules bind to receptor

Front 36

Voltage-gated channels

Back 36

-controlled by voltage difference across cell membrane (ex. Na+, K+, Ca+, Cl-)

-total number of ions that flow through these channels generating ionic current depend on:

1. channel conductance

2. how often the channel is open

3. how long the channel stays open

Front 37

Mechanically-gated channels

Back 37

-susceptible to changes in permeability as they are stressed

Front 38

Carrier-Mediated Transport

Back 38

-specificity: system usually transports one type of molecule

-saturation: rate of transport reaches maximum when all binding sites on transporters are occupied

-competition: occurs when structurally similar substances compete for the same binding site on membrane

Front 39

Facilitated Diffusion

Back 39

-involves presence of carrier molecule that enables solute to penetrate more readily

1. solute binds to carrier

2. carrier undergoes change in configuration

3. solute is delivered to other side of membrane

4. carrier resumes original configuration

Front 40

Active Transport

Back 40

-carrier mediated

-uses energy (usually derived from hydrolysis of ATP)

-susceptible to metabolic inhibitors

-transports against concentration gradient

-primary and secondary

Front 41

Primary Active Transport

Back 41

-in which energy is transferred directly from ATP to transporter

-phosphorylation of transporter changes conformation and affinity of binding site

-changes in bind site affinity for transported solute are produced by dephosphorylation of carrier

Front 42

Na+/K+ Pump Mechanism

Back 42

-carrier binds to Na+ on cytoplasmic surface of membrane

-activates ATPase that hydrolyzes ATP and releases required energy

-carrier changes conformation and delivers Na+ to outer surface

-permits exposure of binding site for K+ on outer surface

-attachment of K+ to its binding site is accompanied by return of carrier to original configuration

-K+ released inside cell

-Na+ binding sites open again

Front 43

Secondary Active Transport

Back 43

-energy released during transmembrane movement of solute from higher to lower concentration is transferred to simultaneous movement of another solute against concentration gradient

-uses electrochemical gradient for Na+ to move both Na+ and second solute across plasma membrane

Front 44

Secondary Active Transport of Na+

Back 44

1. Na+ binds to carrier outside cell (high concentration of Na+)

2. Glucose/amino acids are allowed to bind to same carrier

3. Carrier changes configuration

4. Delivers Na+ and glucose/amino acid into cell

5. Carrier reverts to original configuration and Na+ is extruded from cell via sodium-potassium pump

Front 45

Cotransport

Back 45

-Na+ moves in same direction as solute X

Front 46

Countertransport

Back 46

-Na+ moves in opposite direction as solute X

Front 47

Secondary Active Transport Mechanisms

Back 47

Counter-transport:

-Na+/H+ exchanger

-Na+/Ca2+

-Cl-/HCO3-

Co-transport:

-Na+/glucose cotransporter

-Na+/amino acid

Front 48

Endocytosis

Back 48

-intaking particles into cell

-cell membrane invaginates

-forms channel

-end of channel pinches off to form vesicle

Front 49

Exocytosis

Back 49

-output of particles into ECF

-intracellular vesicle fuses with cell membrane

-contents released

Front 50

Pinocytosis

Back 50

-fluid endocytosis

-ingestion of dissolved materials via endocytosis

-cell membrane invaginates

-pinches off small droplets of fluid in pinocytotic vesicle

-liquid contents slowly transfer to cytosol

Front 51

Phagocytosis

Back 51

-ingestion of solid particles via endocytosis

-cell membrane invaginates

-pinches off

-places particle in phagosome

-phagosome fuses with lysosomes

-material is digested by enzymes

Front 52

Receptor-mediated Endocytosis

Back 52

1. Clathrin-dependent:

-involves pinching off of clathrin-coated vesicles

-fuse with endosomes where contents are sorted

2. Potocytosis:

-clathrin-independent

-pinching off of tiny vesicles called caveolae

-deliver contents to cell cytoplasm via channels/carriers

Front 53

Diffusion of Water

Back 53

-water diffuses freely across most cell membranes

-facilitated by groups of proteins (aquaporins) that form water permeable channels

Front 54

Osmosis

Back 54

-net movement of H2O across a semi-permeable membrane

Front 55

Osmotic Pressure

Back 55

-pressure required to prevent movement of water across semi-permeable membrane

Front 56

Osmolarity

Back 56

-total solute concentration of solution

-1 osmol = 1 mol of solute particles

-Osm = osmol/L

-osmotic pressure is equal to osmolarity (Osm)

Front 57

Isosmotic

Back 57

-solutions with same number of osmotically active particles as normal extracellular solutions

Front 58

Hypoosomtic

Back 58

-solutions with lower number of osmotically active particles than normal extracellular solutions

Front 59

Hyperosmotic

Back 59

-solutions with higher number of osmotically active particles than normal extracellular solutions

Front 60

Hypertonic solution

Back 60

-greater concentration of solute outside cell

-net movement out of water out

-cell shrivels

Front 61

Hypotonic solution

Back 61

-greater concentration of solute inside cell

-net movement of water in

-cell lyses (bursts)

Front 62

Isotonic solution

Back 62

-equal concentrations of solute inside and outside cell

-no net movement of water

Front 63

Capillary Wall

Back 63

-single layer of flattened endothelial cells and supporting basement membrane

Front 64

Transport Across Capillary Wall

Back 64

1. Diffusion

-through water-filled channels and across cell membranes

-most important

2. Pinocytosis/Exocytosis

-endocytosis and vesicle formation on luminal side

-exocytosis and vesicle release on interstitial side

3. Bulk Flow

-flow of molecules subjected to pressure difference

-causes redistribution of extracellular solution

-inversely proportional to hydrostatic pressure differences

-COP of plasma determines how much water will flow in/out capillaries

Starling Forces:

-filtration tends to push out fluid from capillaries

-osmotic flow tends to pull fluid into capillaries

-determine distribution of ECF volume between plasma and ISF

Front 65

Blood pH Range

Back 65

7.30-7.45

Front 66

Blood

Back 66

-supporter of life

-carrier of diseases

-transport

-protective

-comprised of ECF (plasma) and ICF (inside blood cells)

Front 67

Normovolemia

Back 67

-normal blood volume

Front 68

Hypovolemia

Back 68

-lower blood volume

Front 69

Hypervolemia

Back 69

-higher blood volume

Front 70

Composition of Plasma

Back 70

>90% water

-Na+, K+, Ca++, Mg++

-Cl-, HCO3-, PO4--

-glucose, amino acids, lipids, urea, lactic acid

-O2, CO2

-proteins (colloids):

-ablumins

-globulins

-fibrinogen

Front 71

Separating Plasma Proteins

Back 71

1. Differential precipitation by salts

2. Sedimentation in ultracentrifuge

3. Electrophoretic mobility

4. Immunological characteristics

Front 72

Electrophoresis

Back 72

-fractionation method based on movement of charged particles along voltage gradient

-rate of migration is influenced by number of particles and MW of each protein

Front 73

Origin of Plasma Proteins

Back 73

-lymphoid tissue to gamma-Globulin

Front 74

Role of Plasma Proteins

Back 74

-major role in determining distribution of fluid between plasma and ISF compartments by controlling transcapillary dynamics

-contribute to viscosity of plasma

-contribute to buffering power

-fibrinogen and globulins essential to clotting

-immunoglobulins provide specific resistance to infection

-albumin/globulins act as carriers for lipids, minerals and hormones

Front 75

Capillary Bed

Back 75

-site where exchanges take place between plasma and ISF

-diffusion responsible for exchange of nutrients, gases and wastes across capillary wall

-Starling forces determine distribution of ECF volume between plasma and ISF

Front 76

Starling's Transcapillary Dynamics

Back 76

1. Exchanges (filtration/absorption) take place along whole length of capillary

2. Only 90% of fluid filtered out is reabsorbed back into capillary (10% is drained by lympathic vessels)

Front 77

Lymphatic Vessels

Back 77

-walls are made up of single endothelial layer

-highly permeable to all ISF constituents (including proteins)

Front 78

Factors in Transcapillary Dynamics

Back 78

1. Hydrostatic pressure

2. COP

3. Capillary Permeability

4. Lymphatic Drainage

Front 79

Edema

Back 79

-accumulation of excess fluid in interstitial spaces

-high hydrostatic pressure

-low COP

-low capillary permeability

-no lymphatic drainage

Front 80

Elephantiasis

Back 80

-increased capillary permeability

-plasma proteins escape into ISF

-exert oncotic effect

-obstruction of lymphatic drainage

Front 81

Colloidal Osmotic Pressure

Back 81

-colloidal osmotic pressure (COP) = 25mmHg

-if COP increases, net flow into plasma

-COP decreases, net flow into ISF

-COP of plasma determines how much water will flow in/out of capillaries

Front 82

Hematopoiesis

Back 82

-production of blood cells

-all blood cells derived from common, multipotential hematopoietic stem cells

-occurs in flat bones of skull, shoulder blades, vertebrae, pelvis, sternum, ribs, promial epiphysis of long bones

-injection of bone marrow stem cells can reconstitute ALL hematopoietic cell types

Front 83

Erythropoiesis

Back 83

-production of red blood cells

Front 84

Thrombopoiesis

Back 84

-production of platelets

-pluripotent stem cell to commited stem cell

-thrombopoietin from liver

-megakaryocytes

-bone marrow to blood stream

Front 85

Leukopoiesis

Back 85

-production of white blood cells

Front 86

Cytokines

Back 86

-substances (proteins/peptides) released by cell

-affect growth, development and activity of another cell

Front 87

Hematopoietic Growth Factors

Back 87

-cytokines influencing the proliferation and differentiation of blood cell precursors

Front 88

Erythrocytes

Back 88

-red blood cells

-facilitate transport of respiratory gases between lungs/cells

Configuration:

-biconcave disk

-maximal surface area/minimal diffusion distance

-high degree of flexibility

Front 89

Glycolytic Enzymes

Back 89

-generate energy

Front 90

Carbonic anhydrase

Back 90

-CO2 transport

Front 91

Hemoglobin

Back 91

-transport of O2/CO2

-acts as buffer

-low solubility in plasma

-1.34mL O2/g Hb

Affected by:

-temperature

-ionic composition

-pH

-pCO2

-intracellular enzyme concentration

Front 92

Erythropoiesis

Back 92

1. RBC precursor differentiation:

-decrease in size

-loss of nucleus

-accumulation of Hb

2. Reticulocyte to RBC (24 hours)

3. O2 requirements/availability determine number of RBCs

Front 93

Erythropoietin

Back 93

-glycoprotein hormone/cytokine produced by kidney

-stimulates proliferation of committed stem cells

-accelerates differentiation of stem cells into reticulocytes

-release stimulated by hypoxia (decreased RBC count, decreased availability of O2 to blood, increased tissue demand for O2)

Front 94

Hormonal Effects on EPO

Back 94

Testosterone:

-increases release of EPO

-increases sensitivity of RBC precursors to EPO

Estrogen:

-opposite effects

Front 95

RBC Life Span

Back 95

-120 days

-nothing prolongs life span

-recognized as old and removed from circulation by system of macrophages

-old RBC "eaten"

-membrane digested, contents released

Front 96

Jaundice

Back 96

-excessive hemolysis

-hepatic damage

-bile duct obstruction

Front 97

Polycythemia

Back 97

-production of RBCs greater than destruction

-increases blood viscosity

-blood clots!

Front 98

Anemia

Back 98

-production of RBCs less than destruction

-decrease in oxygen carrying capacity of blood

-RBC count/Hb content decreased

Front 99

Physiological Polycythemia

Back 99

-secondary to high O2 needs or O2 availability

-high altitudes

-increased activity

-chronic lung disease

-heavy smoking

Front 100

Pathological Polycythemia

Back 100

-tumours of cells producing EPO

-unregulated production by bone marrow

Front 101

Diminished Production Anemia

Back 101

-abnormal site

-abnormal stimulus

-inadequate raw materials

-ex. Iron Deficiency (most common):

-increased requirements

-inadequate supplies

-microcytic

-hypochromic

Front 102

Ineffective Maturation Anemia

Back 102

-deficiencies of Vitamin B12 and folic acid (required for normal synthesis of DNA)

-macrocytic

-normochromic

Front 103

Increased Destruction Anemia

Back 103

-congenital or acquired

-abnormal membrane structure

-abnormal enzyme systems

-abnormal metabolism

-abnormal Hb structure (ex. sickle cell)

Front 104

Hemorrhage

Back 104

-loss of blood

-external/internal

Front 105

Hematoma

Back 105

-accumulation of blood in tissues

Front 106

Hemostasis

Back 106

-arrest of bleeding

-vasoconstriction

-platelet plug

-blood clot

Front 107

Vasoconstriction

Back 107

-nervous reflex

-myogenic response

-smooth muscle cells in vessel wall respond to injury by contracting

-chemical vasoconstrictors

Front 108

Platelet Structure

Back 108

-2-4 micrometres in diameter

-no nucleus

-many granules

-many filaments, microtubules, mitochondria, sER, etc

-lifespan: 7-10 days

Front 109

Platelet Plug Formation

Back 109

1. Vascular injury, damaged endothelial cell

2. Collagen exposure (binds and activates platelets)

3. Adhesion (facilitated by Von Willebrand factor (wWf)

4. Activation/release of cytokines

-ADP/TXA2 (aggregation/TXA2 promotes vasoconstriction)

-serotonin (promotes vasoconstriction)

-PF3 (source of phospholipid activity that participates in coagulation)

5. Aggregation

6. Consolidation

7. Platelet factors released to attract more platelets

Front 110

Platelet Functions

Back 110

-release vasoconstricting agents

-form platelet plug

-release clotting factors

-participate in clot retraction

-promote maintenance of endothelial integrity

Front 111

Abnormal Primary Hemostatic Response (Prolonged Bleeding)

Back 111

1. Failure of blood vessel to contract

2. Platelet deficiencies

Front 112

Clotting

Back 112

-function of plasma

1. Initiated by injury to blood vessel wall

2. Platelet adhesion

-platelets bind to exposed collagen on endothelial cell surfaces mediated by vWf

3. Platelet Activation

-linking of platelet glycoprotein to collagen activates platelets' integrin

-tight binding of platelets to ECM

-release stored granule contents into blood plasma (ADP, vWf, throboxane, PF3, serotonin)

-platelets aggregate

4. Activation of protein kinase

-calcium activates protein kinase C

-leads to activation of specific phospholipase

-phospholipase modifies integrin membrane glycoprotein making it attracted to fibrinogen

-cross linking between fibrinogen and glycoprotein help platelets aggregate

5. Kalikrien to kinin

-conversion system is a complex of proteins that leads to formation of vasoactive kinins

-kinins released as result of activation of tissue kallikrein or plasma kallikrein

6. Blood coagulation cascade

-process of fibrin formation takes place in intrinsic and extrinsic pathways

7. Prothrombin to thrombin

-Ca2+/prothrombinase catalyze

8. Control of thrombin

-small amounts of thrombin generated rapidly by extrinsic scheme

-trigger strong positive feedback effects on intrinsic scheme to generate larger quantities of thrombin

9. Activation of fibrinogen to fibrin

-catalyzed by thrombin formation

10. Clot Retraction/Lysis

-clotting kept in check by inhibitors (plate adhesion) and anticoagulants

-heparin/antithrombin II work together to block IX, X, XI, XII

-protein C inhibits Factors V and VIII

Front 113

Clotting Factors

Back 113

-Ca2+

-phospholipids

-protein plasma factors

Front 114

Clotting Factor Deficiences

Back 114

Congential:

-hereditary deficiencies of (usually) a single factor

-ex. VIII (hemophilia)

Acquired:

-multifactor deficiencies

-ex. liver disease, vitamin K deficiency

Front 115

Clot Retraction

Back 115

-depends on presence of contractile protein (thrombosthenin) released by platelets

Front 116

Clot Lysis (Fibrinolysis)

Back 116

-intrinsic/extrinsic proactivators/endothelial cell factors to plasminogen activator

-plasminogen to plasmin

-fibrin to fibrin fragments

1. Inhibitors of platelet adhesion (ex. aspirin)

2. Anticoagulant drugs interfere w/ clot formation

3. Thrombolytic drugs (promote clot lysis)

Front 117

Coumarin

Back 117

-anticoagulant drug

-blocks synthesis of functional prothrombin, VII, IX, X

Front 118

Heparin

Back 118

-promotes inhibition of thrombin activation/action

Front 119

Tissue Plasminogen Activator (t-Pa)

Back 119

-thrombolytic drug

-promotes clot lysis

Front 120

Streptokinase

Back 120

-thrombolytic drug

-promotes clot lysis

Front 121

SCIDs

Back 121

-severe combined immunodeficiency

-bubble boy

-lead to discovery that thymus, lymph nodes and bone marrow were important in immune system

Front 122

Primary Organs of Immune System

Back 122

-stem cells from yolk sac

-to fetal liver

-bone marrow

-thymus gland

-formed in utero

Front 123

Secondary Organs of Immune System

Back 123

-lymph nodes

-spleen

-mucosa-associated lymphoid tissue (MALT)

-formed in utero

Front 124

Antigen

Back 124

-dangerous!

-immunogen

-hapten (+ carrier = immunogen)

-allergen

-tolerogen

-ligand

Front 125

3 Lines of Defenses

Back 125

1. Coverings of body (skin/mucous membranes)

2. Innate Immune Response

3. Acquired Immune Response

Front 126

Humoral vs Cellular Immunity

Back 126

Humoral:

-antibodies produced by lymphocytes

-circulating freely in body fluids

-bind temporarily to target cell

-mark for destruction by phagocytes or complement

Cellular Immunity:

-lymphocytes act against target cells

-directly: killing infected cells

-indirectly: releasing chemicals to enhance inflammatory response

-cellular targets

Front 127

Skin and Mucous Membranes

Back 127

-unpleasant for microorganisms

Front 128

Fixed Tissue Macrophages

Back 128

-first cell to be activated when first line of defence is breached

-toll like receptors (TLR)

-sees PAMPs (pathogen associated molecular patterns) on bacteria

-binds to PAMPs

-sends out MDNCF signals to neutrophils

Front 129

PAMPs

Back 129

-pathogen associated molecular patterns

-particular to bacteria

-foreign to body

Front 130

Innate Immune Response

Back 130

-second line of defense

-early in evolution

-acts quickly

-cellular/humoral

-no memory

-results in inflammation

Front 131

Cellular Factors of Innate Immunity

Back 131

-phagocytic cells:

-neutrophils, macrophages, dendritic cells

-cells w/ inflammatory mediators:

-basophils, mast cells, eosinophils

Front 132

Humoral Factors of Innate Immunity

Back 132

-acute phase reactants (ex. C-Reactive Protein, Complement, Interleukin, etc)

-cytokines

Front 133

Myeloid cells

Back 133

-white cells

-polymorphs (neutrophils)

-monocytes (macrophages and dendritic cells)

-lymphoid system (lymphocytes)

Front 134

Person Steps on Broken Glass!

Back 134

-macrophage sends out MDNCF signal to neutrophils

-neutrophils kill bacteria

-neutrophil extracellular traps (NETs)

-dendritic cell arrives

-picks up bacteria on surface

-digests some

-dendritic cell returns to lymph node

Front 135

Diapedesis

Back 135

-neutrophil slips capillary wall

Front 136

Neutrophil Extracellular Traps (NETs)

Back 136

-net of cytotoxic material that tries to trap bacteria and prevent it from developing sepsis

Front 137

Neutrophil Action

Back 137

-reacts to MDNCF signal sent by macrophage

-rolls around capillary

-changes molecular structure with capillary wall

-adhesion to capillary wall

-diapedesis

-makes way through tissue via chemotaxis

-kills bacteria via phagocytosis

-commits suicide

-produces pus and NETs

Front 138

Natural Killer Cell

Back 138

-has to be turned on

-all normal cells have natural killer cell activating ligands

-MHC Class I molecules turn off natural killer cells

-altered/absent MHC Class I cannot stimulate negative control

-once NK is triggered it induces apoptosis in target cell

Front 139

Classical Pathway

Back 139

1. Antigen/antibody complexes

2. Complement Activation

3. Recruitment of Inflammatory cells (neutrophils)

Front 140

MB-Lectin Pathway

Back 140

1. Lectin binding to pathogen surfaces

2. Complement Activation

3. Oponisation of pathogens (coats them and makes them tasty!)

Front 141

Alternative Pathway

Back 141

1. Pathogen surfaces

2. Complement activation

3. Killing of Pathogens (blow hole in them!)

Front 142

Inflammation

Back 142

-rubor (redness)

-calor (heat)

-dulor (pain)

-tumor (sweling)

Front 143

Acquired Immune Response

Back 143

-humoral (immunoglobulin/antibody mediated)

-cell-mediated (T cell/lymphocyte effector)

-specific with memory

-Tc, Th, ILs, Ig, B-cilia, etc

Front 144

Processes of Immune Response

Back 144

Early Processes:

-events that initiate immune response

-interaction between innate and acquired

-Th (CD4+)

-cellular and humoral processes

Late Processes:

-"killing" aspect of immunity

-humoral response: antibodies

-cellular response: Tc cells (CD8+)

Front 145

Major Compatibility Complex

Back 145

-H2 (mouse)

-HLA complex (human)

-rejects foreign tissues (transplants do not occur naturally)

-involved in immune responses

-two molecular classes:

-MHC I

-MHC II

Front 146

MHC I

Back 146

-HLA-A

-HLA-B

-HLA-C

-large alpha chain

-small beta chain

-all cells have HLA MHC Class 1 molecule action

Front 147

MHC II

Back 147

-HLA-DP

-HLA-DQ

-HLA-DR

-alpha and beta chains roughly the same size

-only in dendritic, macrophage, B lymphocyte cells

-presents antigens

-groove for antigenic fragment

Front 148

Dendritic Cells

Back 148

-link between adaptive and innate immune systems

-"picks up" remainder of bacteria after neutrophils

-travels back to lymph nodes in groin

-phagocytosis/digestion takes place

-antigen presentation: MHC II molecules

-brings antigen fragments from phagosome to peptide-binding groove in MHC II molecule

-specific interaction between MHC peptide and T cell receptor

-B7 links to CD28 on T cell

Front 149

B cells

Back 149

-production of antidbodies

-each can only make one antibody

-educated in bone marrow

-make way to regional lymph nodes:

-live in superficial cortex

Front 150

T cells

Back 150

-thymus

-Th2 (CD4+)

-cytotoxic T cell (CD8+)

-regulatory T cell (CTLA4)

-Th1

-Th17

-Th3

-NKT

-95% die in thymus

-make way to regional lymph nodes:

-live in deep cortex/medulla area

Front 151

Checkpoint Inhibition

Back 151

1. All bio activities have shut off controls

2. Immunogenic response involves displacement of CD28 from B7 by:

a. CTLA4

b. PD-1

Front 152

Peripheral Tolerance

Back 152

-occurs at same time as initiation of immune response

-dendritic cell has taken up peptide

-T helper cell binds to MHC Class II and B7

-regulatory T cell downregulates immune response

Front 153

Regulatory T cell

Back 153

-CTLA4

-downregulates immune response

-prevents you from becoming autoimmune

Front 154

Initiation of Acquired Immune Response

Back 154

1. B Cell binds to dendrite (surface antigen/specific immunoglublin) and T helper cell (CD40L)

2. Th2 cell produces IL 4, 5 and 6

3. Interleukins expand B cell family

-produce clones programmed for specific antibody

4. Shut off takes place by displacement of B7 by CTLA4 or PD-1

Front 155

Antibodies

Back 155

-immunoglobulins

-monomeric structure:

-four chains (tetrapeptide)

-two light chains determine type (Kappa/Lambda)

-two heavy chains determine class (Delta, Mu, Epsilon, Gamma, Alpha)

-bound by disulfide bonds (inter/intrachain)

-Fab sites = antigen binding fragment (at hypervariable regions)

-Fc sites = crystallizable fragment determines biological activity of molecule (IgM, IgG, IgA, IgE)

Front 156

IgM

Back 156

-pentomeric

-first antibody class to be produced

-good at complement binding

-cumbersome

Front 157

IgG

Back 157

-placental transfer

-complement binding

Front 158

IgA

Back 158

-secretory properties (MALT)

Front 159

-IgE

Back 159

-mastocytophilic properties

Front 160

Complement Cascade

Back 160

1. First molecule to bind to Fc sites between Ig heavy chains is C1q

2. Second molecule is C4

3. Followed by C2, C3, C5...

4. C3 breaks down to C3a/C3b and coats bacteria

5. C5 breaks down to C5a/C5b and signal neutrophils (chemotactic) with C3

6. C9 punches hole on bacteria surface

Front 161

Paul Ehrlich

Back 161

-Pauling was wrong

-all cells live through receptors on surface

-side-chain theory for antibody production

-cell recognizes small amount of antigens

-produces lots of antibodies

-antibodies circulate in blood

Front 162

B cell series

Back 162

1. Pro-B

-primitive

-from thymus/bone marrow

2. Pre-B

-surface immunoglobulin marker

-expresses RAG1/2

3. Mature B cell

-mature immunoglobulin marker (specific)

-returns to bone marrow

-expresses RAG1/2 (?)

4. Plasma Cell

-produces antibodies

-loses immunoglobulin marker

5. death

Front 163

Tonegowa

Back 163

-lots of antibodies not a lot of genes

-random creation of molecules (body doesn't know what its going to need yet)

-95% are killed, 5% become specific to antigens

-class switching (ex. between IgG and IgM)

Front 164

Immune Response Memory

Back 164

-used antibodies undergo apoptosis

-memory cells stored in apical light zone of lymph nodes

-rapid antibody production after secondary exposure to antigen

-eventually production of antibodies declines

Front 165

Th1

Back 165

-T helper cell 1

-produces INF and IL 2

-acts with CD8+ killer cell

Front 166

Th2

Back 166

-produces IL 4, 5, 6

Front 167

Th17

Back 167

-upregulates immune response

Front 168

Th3

Back 168

-involved in mucosal immunity

-protects mucosal surface in gut from nonpathogenic non-self antigens

-inhibits Th1/Th2

Front 169

Viral Infection

Back 169

1. Virus invades

-goes to tissue from where it was made in nature

2. Taken up by dendritic cell

-may or may not get stuck on surface

-chopped up

-dendritic cell presents MHC Class I molecule w/ antigenic peptide and B7

3. Th1 cell binds

-produces INF and IL2 cytokines

-expand cytotoxic T cell population

4. Humoral antibody made against antigenic fragment

Front 170

Proteasome

Back 170

-used cells are put through proteasome in order to reuse materials

-virus goes to surface of dendritic cell in MHC Class I molecule using proteasome mechanism

-bypasses T cell help

-shown directly to CD8+ cell

Front 171

Tolerance

Back 171

-95% of cells in thymus are destroyed

-T cells that don't recognize MHC Class II molecules are destroyed

-T cells that recognize MHC Class II self-peptide complexes are negatively selected

-T cells that recognize MHC Class II non-self-peptide complexes are positively selected and peripheralized to secondary lymphoid organs

Front 172

Maintenance of Tolerance

Back 172

1. Inactivation of co-stimulatory signals (B7/CD80 and 86)

2. Regulatory T cell inhibits Th activation

3. Clonal Anergy

Front 173

Ferritin

Back 173

-iron-storing/releasing protein

Front 174

Bilirubin

Back 174

-product that occurs in breakdown of heme

-gives bile distinct brownish-yellow color

Front 175

Pernicious anemia

Back 175

-Vitamin B12 deficiency

Front 176

Intrinsic Pathway (Clotting)

Back 176

1. Activation of Factor XII

2. Release of platelet phospholipids (containing PF3)

3. Activated Factor XII activates XI

-requires kininogen

-accelerated by prekallikrein

4. Factor XIa enzymatically activates Factor IX to IXa

-with Ca++

3. Factor IXa + VIIIa + platelet phospholipids form prothrombin activator

4. Prothrombin activator initiates cleavage of prothrombin to form thrombin

-takes longer than extrinsic

Front 177

Extrinsic Pathway (Clotting)

Back 177

1. Release of Tissue Factor

2. Activation of Factor X

-tissue factor complexes with Factor VII in presence of Ca+

3. Factor Xa forms prothrombin activator

-in presence of Ca+

-combines with tissue/platelet phospholipids/Factor V

Front 178

Skeletal Muscle

Back 178

-striated, long thin multinucleated cells

-composed of long bundles of muscle fibers (myofilbrils)

-generated during development by fusion of myoblasts

-most abundant type of muscle in body

-used for posture/locomotion

-enables arms/legs to contract voluntarily

Front 179

Cardiac Muscle

Back 179

-striated

-responsible for rhythmic contractions of heart

-involuntary contractions

Front 180

Smooth Muscle

Back 180

-non-striated

-causes involuntary contraction in blood vessels, gut, bronchi and uterus

-involves thick filaments pulling on thin filaments (similar to skeletal)

-actin/myosin lack highly ordered structure (sarcomeres)

Front 181

Myofibrils

Back 181

-bundle of muscle fibers

-striped

-I bands: light stripes

-A bands: dark stripes

-Z-line: dark line in the middle of I band

-H-zone: lighter zone within A band

-M-line: middle of H zone

-thick and thin filaments

Front 182

Myosin thick filaments

Back 182

-extend from A band to A band

-myosin: fibrous protein

-head groups

-1 thick filament consists of 2 myosin bundles w/ head groups orientated in opposite directions

-M line is where myosin bundles are attached

Front 183

Actin thin filaments

Back 183

-attached to Z lines and extend across I band partway into A band

-each actin filament forms from two chains of globular actin subunits

-twisted into helix

Front 184

A band

Back 184

-dark stripes

-lattice of thick/thin filaments

-each thin filament surrounded by three thick filaments

Front 185

H zone

Back 185

-lighter zone within A band

-only thick filaments, no overlapping thin filaments

Front 186

Length Tension Relation

Back 186

-reflects degree of overlap between thick/thin filaments

-muscle contraction: maximal tension rises

Front 187

Sliding Filament Model

Back 187

-head groups reach out and grab, pull and release thin filaments repeatedly

-pulls thin filaments over thick filaments

-Z lines closer together

-driven by ATP hydrolysis

Front 188

Cross-bridge

Back 188

-where thick filaments interact w/ thin filaments

Front 189

Cross-bridge Cycle

Back 189

1. Myosin head group binds ATP

2. Head group releases actin thin filament

3. Hydrolyzes ATP, releases energy

4. Energy used to push back head group (stretched, energy stored)

5. Binds to actin filament again

6. Undergoes conformational change

7. ADP/phosphate released as myosin head pulls thin filament forwards

Front 190

Rigor Mortis

Back 190

-animal dies

-ATP supplies decrease

-myosin head groups cannot release thin filaments

-stuck in pulled position (stiff muscle)

Front 191

Motor Unit

Back 191

-motor neuron and group of muscle fibers it innervates

-motor neurons in ventral part of spinal cord

-axons exit from dorsal side

-each motor neuron goes to specific muscle

-axons can branch to multiple fibers

-multiple muscle fibers are innervated by a single motor neuron

Front 192

Neuromuscular Junction Structure

Back 192

-very large synapse

-neurotransmitter released: Acetylcholine (ACh)

-nACh receptors found in post-synaptic membrane (end plate)

-end plate is small specialized region w/ junctional folds

Front 193

Neuromuscular Transmission

Back 193

1. Action potential in motor neuron

2. ACh released at presynaptic terminal

3. Binds to nACh receptors

4. Ion channel opens

5. Influx of sodium, generates depolarization

6. Action potential propagates from end plate down to ends of muscle fibers.

7. Muscle fiber is coated w/ voltage gated channels, contracts as single unit.

-resting potential of end plate is very large, always large enough to push past action potential

Front 194

Sarcoplasmic Reticulum

Back 194

-intracellular compartment that stores calcium ions

Front 195

T-tubules

Back 195

-where membrane extends down into muscle fibers

-holes in membrane, continuous w/ external environment

-allows outside of cell to communicate w/ inner

Front 196

Excitation-Contraction Coupling

Back 196

1. Action potential propagates down muscle fiber membrane

2. Reaches t-tubule

3. Depolarizes membrane of t-tubule

4. Activates voltage gated DHP receptor (calcium ion channel). Conformational change.

5. Influx of calcium into cell (from sarcoplasmic reticulum--not t-tubule).

6. Increase in intracellular calcium concentration gives signal to contract. Direct physical coupling w/ Ryanodine receptor.

7. Calcium released from SR binds to troponin on thin filaments.

8. Conformational change in troponin.

9. Associated tropomyosin (wrapped around thick filament) is moved away from myosin binding site on actin.

10. Myosin binding site on actin can now bind to heads of thick filaments.

11. Myosin head group cycling proceeds.

Front 197

Twitch

Back 197

-contraction of a muscle fiber in response to a single action potential

-very quick

-action potential is finished before contraction even begins (delay due to excitation-contraction coupling)

-duration of contraction reflects time it takes for [Ca++] to return to baseline

Front 198

Generation of Muscle Tension

Back 198

-force generated by muscle = tension

-tension exerted by whole muscle is controlled by recruitment and summation

-skeletal muscle is adapted for large force generation over narrow operating range

-summation: additive effects of several closely spaced twitches

-recruitment: additional motor units, increasing muscle tension

Front 199

Skeletal Muscle Energy Metabolism

Back 199

-not a lot of premade ATP

-can transfer P from creatine phosphate by creatine kinase to ADP to create ATP for a few seconds of muscle activity

-levels of ATP are sustained during prolonged muscle activity by glycolysis and oxidative phosphorylation

-glycogen in muscle and glucose/fatty acid from blood provide fuel

Front 200

Glycogen

Back 200

-polysaccharide comprising of long chains of glucose molecules

-stored energy in muscle fibers

Front 201

Glycolysis

Back 201

-glucose (blood)/glycogen (muscle fiber) to ATP

-waste product: lactic acid

Front 202

Oxidative Phosphorylation

Back 202

-oxygen/fatty acids from blood to ATP

-glycogen/glucose can undergo glycolysis and then oxidative phosphorylation to produce ATP

Front 203

Fast Glycolytic Muscle Fibers

Back 203

-myosin with high ATPase activity

-no myoglobin ("white muscle")

-energy mainly comes from creatine phosphate and glycogen (glycolysis step only)

-generation of large force over short periods of time

-not energy efficient (rapid lactic acid buildup)

Front 204

Slow Oxidative Muscle Fibers

Back 204

-myosin with low ATPase activity

-myoglobulin to facilitate O2 transport from blood ("red muscle")

-generate ATP through glycolysis and oxidative phosphorylation

-generation of low force over prolonged time period

-more energy efficient

Front 205

Fast Oxidative Muscle Fibers

Back 205

-intermediate properties

-fast myosin and oxidative metabolism

Front 206

Muscle Fatigue

Back 206

-protects from damage

-in fast glycolytic fibers: due to lactic acid an changes in ion gradients (increase in extracellular K+) that affect action potentials

-in slow oxidative fibers: depletion of glycogen?

Front 207

Anaerobic Muscle Response

Back 207

-anaerobic activity: high intensity, short duration

-muscles increase in diameter (fast glycolytic fibers)

-hypertrophy

-ex. bodybuilders

Front 208

Aerobic Muscle Response

Back 208

-aerobic activity: low intensity, long duration

-increase in fiber mitochondria

-increased vascularization

-increased ability of muscle fibers to extract ATP via oxidative metabolism

-muscles do not become stronger or bigger

Front 209

Smooth Muscle Contraction

Back 209

1. Activated by Ca++ released from SR or flowing into cell via membrane Ca channels

2. Ca++ binds to calmodulin

3. Activates myosin light chain kinase

4. Kinase phosphorylates, activating SM myosin.

-smooth muscle activity is regulated by extracellular signals (ex. hormones, neurotransmitters of ANS)

Front 210

Synapses

Back 210

-communication sites between neurons

-human nervous systems contain a LOT of synapses

Front 211

Soma (Neuron)

Back 211

-cell body

-keeps neuron alive

-can chop off dendrites/extensions and neuron can still survive

Front 212

Dendrites (Neuron)

Back 212

-branching off soma

-channel input/output

-dendritic spines increase surface area of dendrites

-often ribosomes present that allow spine to remodel shape in response to varying synaptic activity (learning/memory?)

Front 213

Axon (Neuron)

Back 213

-region of axon that arises from cell body is the initial segment/axon hillock (trigger zone)

-axons may have branches (collateral)

-greater degree of branching = greater influence

-branches end in presynaptic termianls

-many axons are covered in myelin

Front 214

Presynaptic Terminals (Neuron)

Back 214

-axon branches end in presynaptic terminals

-become dendrites of another neuron

-responsible for releasing neurotransmitters from axon

Front 215

Ogliodendrocytes

Back 215

-myelin-forming cells in brain/spinal cord

-type of glial cell

Front 216

Schwann cells

Back 216

-form myelin sheaths at regular segments around axons in PNS

-type of glial cell

Front 217

Glial Cells

Back 217

-surround soma, axon and dendrites of neurons

-provide physical and metabolic support

-no information processing function

-retain capacity to divide throughout life

Front 218

Astrocytes

Back 218

-type of glial cell

-regulate composition of ECF in CNS by removing K+ and neurotransmitters (ex. glutamate) around synapses

-support for capillaries

-also stimulate formation of tight junctions in blood-brain barrier

Front 219

Microglia

Back 219

-type of glial cell

-macrophage-like

-perform immune functions in CNS

-may contribute to synapse remodeling/plasticity

Front 220

Ependymal Cells

Back 220

-type of glial cell

-line fluid-filled cavities within brain/spinal cord

-regenerate production and flow of cerebrospinal fluid

Front 221

Neural Growth

Back 221

1. Begins in embryo with division of stem cells

2. Neuronal daughter cells migrate to final location.

3. Send out processes that become axons/dendrites

4. Growth cones form the tip of extending axons.

5. As axon grows it is guided by other cells (usually glial cells)

6. Once target of growth cone is reached synapses form.

-synapses are active before final maturation

Front 222

Plasticity (Nervous System)

Back 222

-ability of brain to modify its structure/function in response to stimulus/injury

-involves generation of new neurons/remodeling of synaptic connections

-highly active excitatory synapses can become stronger

-stimulated by exercise/engaging in cognitively challenging activities

-varies w/ age (younger = more plasticity)

Front 223

Resting Membrane Potential

Back 223

-inside of neuron is slightly more negative than outside (-60/-70mV)

-membrane is selectively permeable to K+ at rest

-high concentration of K+ inside cell/Na+ outside

-concentration gradient pulls K+ outside cell (more positive outside)

-accumulation of unpaired electrons inside creates electrical gradient

-K+ pulled back inside cell

-at equilibrium the concentration gradient = electrical gradient

Front 224

Graded Potentials

Back 224

-charges in membrane potential confined to small regions of plasma membrane

-usually produced when specific change in cell environment acts on specialized region of membrane

-magnitude is graded

-no threshold or refractory period

Front 225

Action Potential

Back 225

-transient depolarizing spike that moves down axon

-propagates down length of axon to presynaptic terminals

-action potential initiated when membrane is depolarized past threshold level

-threshold is usually 20mV greater than resting potential

-all or none phenomenon

Front 226

Synaptic Potential

Back 226

-graded potential change produced in postsynaptic neuron in response to release of neurotransmitter by presynaptic

-depolarizing or hyperpolarizing

Front 227

Receptor Potential

Back 227

-graded potential at peripheral endings of afferent neurons in response to stimuli

Front 228

Threshold Potential

Back 228

-membrane potential at which action potential is initiated

Front 229

Voltage Gated Sodium Channels

Back 229

-closed at resting potential

-delayed activation contribute to falling phase of action potential

-repolarization occurs faster

Front 230

Absolute Refractory Period

Back 230

-brief period after action potential when membrane is un-excitable

Front 231

Relative Refractory Period

Back 231

-over longer time period during which voltage gated K+ channels are open, membrane potential overshoots resting level

-axons are less excitable and unlikely to fire action potentials

Front 232

Tetrodotoxin

Back 232

-poision (ex. puffer fish)

-extremely potent inhibitor of sodium channels

-binds to outer opening of sodium channel, blocking it

-neurons can't propagate action potential

-also blocks sodium channels responsible for skeletal muscles (mainly diaphragm)

-high potency

Front 233

Batrachotoxin

Back 233

-ex. Phyllobates frogs

-sodium channel activator

-irreversibly opens Na+ channels

-constant propagation of axon potentials

-massive seizures

-less potent (doesn't need to be)

Front 234

Effect of Therapeutic Drugs On Sodium Channels

Back 234

-block sodium channels, inhibit axons from firing action potentials

-much less potent than tetrodotoxin

Front 235

Myelination

Back 235

-myelin wrapped around axons

-acts as an electrical insulator

-enables higher conduction velocity

-periodic gaps in myelin (nodes of Ranvier)

Front 236

Nodes of Ranvier

Back 236

-periodic gaps in myelin

-contain high concentration of voltage-gated Na+ channels

-enables signal to be regenerated at periodic intervals

-spreads down farther and faster since there are no Na+ channels in myelin covered areas

Front 237

Multiple Sclerosis

Back 237

-lesions in cerebral cortex

-degraded myelin during episodes

-myelin can recover initially but over the years it gradually worsens

Front 238

White Matter

Back 238

-corresponds to regions of brain that contain mostly myelinated axons

-axons run in clearly defined tracts

Front 239

Gray Matter

Back 239

-comprises cell bodies, dendrites and synapses

Front 240

Axodendritic Synapses

Back 240

-presynaptic makes connection with spine synapses

-shaft synapses are often inhibitory

-axodendritic synapses are abundant

Front 241

Axosomatic Synapses

Back 241

-presynaptic makes connection on cell body

-often inhibitory

Front 242

Axoaxonic Synapses

Back 242

-presynaptic terminal of one axon makes synapse onto presynaptic terminal of another axons

-modulates activity of presynaptic terminal

-can inhibit/facilitate neurotransmitter release

ex. inhibition of pain signals in spinal cord

1. Stimulus cause pain afferents to fire into synapses, traveling up spinal cord to brain stem

2. Descending regulation of neurotransmitters at spinal cord.

3. Axoaxonic endorphin neurons release endorphins onto presynaptic terminals. Inhibts release of neurotransmitters signalling pain.

Front 243

Structure of Synapse

Back 243

-postsynaptic and presynaptic terminals separated by synaptic cleft

-presynaptic vesicles within presynaptic terminals

-vesicles in active zone are lined up facting synaptic cleft

-high postsynaptic density in postsynaptic spine directly across from active zone

Front 244

Neuromodulators

Back 244

-ex. dopamine, serotonin, norepinephrine, endorphins

-usually modify postsynaptic cell's response to specific neurotransmitters

-modulate global neural states (alterness, attention, mood)

-receptors of neuromodulators are often metabotrophic

-neurons that release neuromodulators often originate in brainstem/midbrain nuclei

-axons project diffusely throughout brain

Front 245

Acetylcholine (ACh)

Back 245

-major neurotransmitter in PNS

-neurons that release ACh are cholinergic

-ACh is synthesized from choline and acetyl coenzyme A

-stored in synaptic vesicles

-after release it activates receptors on postsynaptic membrane

-acetylcholinesterase rapidly destroys ACh at postsynaptic membrane (releases choline and acetate)

-choline can be sent back to presynaptic terminal for recycling

Front 246

Catecholamines

Back 246

-ex. dopamine, norepinephrine, epinephrine

-broken down at ECF and axon terminal by monoamine oxidase (MAO)

-drugs used to treat mood disorders are usually MAO inhibitors

Front 247

Serotonin

Back 247

-produced from tryptophan

-slow onset of effects (neuromodulator)

-in general: excitatory effect on pathways involved in muscle control

-inhibitory effect on pathways that mediate sensations

Front 248

Glutamate

Back 248

-common excitatory amino acid

-primary neurotransmitter at 50% of excitatory synapses in CNS

-AMPA and NMDA receptors

Front 249

GABA

Back 249

-major inhibitory neurotransmitter in brain

Front 250

Glycine

Back 250

-major neurotransmitter released from inhibitory interneurons in spinal cord/brainstem

-binds to ionotrophic receptors, allows Cl- to enter postsynaptic cells

-hyperpolarizes

Front 251

Chemical Synaptic Transmission

Back 251

1. Action potential invades presynaptic terminal

2. Ca++ channels open. Influx of Ca++ into terminal

3. Synaptic vesicles in active zone fuse w/ presynaptic membrane.

4. Neurotransmitter released into synaptic cleft.

5. Neurotransmitters diffuse across synaptic cleft and activate postsynaptic ligand gated ion channels

6. Ion channels open, influx of ions into cell.

7. Change in electrical properties of post synaptic cell.

Front 252

Effect of Neurotoxins on Synaptic Transmission

Back 252

-change in [Ca++] in presynaptic terminal is detected by protein complex binding vesicles to active zone

-ex. botox, tetanus contain proteases

-toxins taken up by presynaptic terminals of motor neurons

-proteases digest protein complex and prevent vesicles from fusing w/ presynaptic terminal

-synapses are non functional (no muscle contraction)

Front 253

Excitatory Synapses

Back 253

-mostly on spines of dendrites

-neurotransmitter released is usually glutamate

-two main kinds of ionotropic glutamate receptors (AMPA/NMDA)

-postsynaptic response is an excitatory postsynaptic potential (EPSP)

-postsynaptic membrane is depolarized

Front 254

AMPA receptors

Back 254

-ionotrophic glutamate receptor on postsynaptic cell

1. Glutamate binds to receptor

2. Pore on receptor is permeable to Na+. Influx of Na+ into postsynaptic cell

3. Small transient depolarization of postsynaptic spine. Too small to depolarize intial segment to threshold

4. 50 to 100 EPSPs must sum at initial segment to generate action potential.

Front 255

NMDA receptors

Back 255

-ionotrophic glutamate receptors on postsynaptic cell

1. Glycine and glutamate bound to receptor blocked by Mg++ at resting membrane potential.

2. Depolarization expels Mg++, enabling pore to conduct.

3. Open pore is permeable to Ca++ and monovalent cations

4. Glycine is no longer bound to receptor

-act as coincidence detector (glutamate as bound to receptor and postsynaptic terminal has been depolarized)

Front 256

Long-Term Potentiation

Back 256

-model of synaptic plasticity

1. Stimulus pulse to presynaptic cell generates action potential. Ca++ released. Neurotransmitter released.

2. AMPA receptors open. Influx of Ca++ into postsynaptic cell.

3. Postsynaptic spine is depolarized.

4. Removal of Mg++ blocking NMDA receptors. Larger Ca++ influx into postsynaptic spine.

-EPSPs are larger after single action potential hours after induction of LTP

-synapse is stronger

-learning/memory

Front 257

Excitotoxicity

Back 257

-high concentrations of glutamate are toxic to neurons

-[Ca++] too high in postsynaptic cell

-cell commits suicide

-ex. during a stroke, blood supply to portion of brain is lost

-neurons die

-glutamate released, surrounding neurons die due to excitotoxicity

Front 258

Inhibitory Synapses

Back 258

-main neurotransmittor is GABA

-post synaptic receptor responsible for IPSP: GABA-alpha receptor

Front 259

GABA-alpha receptor

Back 259

-ionotropic GABA receptor

-activation causes influx of Cl-

-hyperpolarizes postsynaptic membrane

-potentiated by variety of drugs (ex. benzodiazepines, barbiturates, ethanol)

-enhance inhibitory activity of synapses, make you sleepy!

Front 260

Metabotrophic Receptors

Back 260

-G-protein coupled receptors

-glutamate synapses have both ionotrophic and metabotrophic glutamate receptors

1. When glutamate binds to metabotrophic receptors it changes their conformation

2. Receptor is activated. Generates chemical signal (second messenger) in postsynaptic cell.

3. 2nd Messengers activate range of cellular proteins. 2nd messengers diffuse around cell, change biochemistry.

4. Long term changes in postsynaptic cell

-at inhibitory synapses there are also metabotrophic GABA-beta receptors

Front 261

Autonomic Nervous System

Back 261

-sensory and motor system

-made up of two neurons connecting CNS and effector cells

-innervates visceral tissues and organs (not skeletal muscle)

-divided into sympathetic, parasympathetic and enteric systems

-sympathetic and parasympathetic innervate cardiac, smooth muscle and glandular tissue

-work in opposition to regulate

Front 262

Sympathetic ANS

Back 262

-form thoracic and lumbar regions of spinal cord

-fight or flight

-increased breathing, raised heart rate, sweating, etc

-most sympathetic ganglia lie close to spinal cord and form sympathetic trunks (2 chains of ganglia) which increase activity to occur body wide

Front 263

Parasympathetic ANS

Back 263

-brainstem/sacral portion of spinal cord

-rest/digest

-slows heart and breathing, increases metabolic function

-tend to activate specific organs in finely tailored pattern given the physiological situation

-includes Vagus nerve

Front 264

Enteric System

Back 264

-controls digestive tract where autonomic neurons innervate nerve network of intestinal wall

-includes sensory neurons and interneurons

Front 265

Preganglionic Neurons

Back 265

-in ANS

-neurons passing between CNS and autonomic ganglion

-neurotransmitter released between pre and post ganglionic neurons is ACh

Front 266

Postganglionic Neurons

Back 266

-in ANS

-connect ganglia and effector cells

-in parasympathetic: neurotransmitter released between postganglionic neuron and effector cell is ACh

-in sympathetic: norepinephrine

Front 267

Effects of Nicotine

Back 267

-stimulation and desensitization of nicotinic ACh receptors at autonomic ganglia

-low doses: nicotine activates autonomic ganglia and stimulates release of catecholamines from adrenal medulla

-sympathetic effects dominate control of cardiovascular system:

-heart rate/b.p. increases

-parasympathetic effects dominate control of GI tract:

-activation of smooth muscle motor activity

-higher doses: brainstem control centers that regulate GI functions can overactivate (vomiting/diarrhea)

Front 268

Central Nervous System

Back 268

-brain/spinal cord

Front 269

Peripheral Nervous System

Back 269

-transmit signals between CNS and receptors/effectors in all other parts of body

-somatic and autonomic parts (somatic innervates skeletal muscle cells)

Front 270

Afferent

Back 270

-sensory input

-cell bodies outside CNS

Front 271

Efferent

Back 271

-motor output

-cell bodies in CNS

Front 272

Divisions of Spinal Cord

Back 272

Cervical Nerves

-8 pairs

-neck, shoulders, arms and hands

Thoracic Nerves

-12 pairs

-shoulders, chest, upper abdominal wall

Lumbar Nerves

-5 pairs

-lower abdominal wall, hips and legs

Sacral Nerves

-5 pairs

-genitals and lower digestive tract

Coccygeal Nerves

-1 pair

Front 273

Spinal Cord Anatomy

Back 273

-31 spinal segments

-each segment has pair of nerves on each side

-dorsal horns: afferents

-ventral horns: efferents

-dorsal roots: afferent (dorsal root ganglion)

-ventral root: efferent (motor axons)

Front 274

Early Development of Nervous System

Back 274

-fertilized egg (ovum)

-ball of cells

-blastocyst

-week one: inner cell mass

-week three: embryonic disk w/ neural plate

-embryonic disk has 3 layers:

-ectoderm (develops into CNS)

-mesoderm (muscle/other tissues)

-endoderm (digestive tract)

Front 275

Neural Tube Development

Back 275

-forms in between week 3 and 4

-neural tube becomes CNS and part of PNS

-neural crest becomes part of PNS

-specialized during week 4

-vesicles develop (forebrain, midbrain, hindbrain)

-forebrain develops into cerebral hemispheres and thalamus

-hindbrain develops into cerebellum, medulla and pons

-remainder of neural tube stretches to form spinal cord

Front 276

Ventricles (Brain)

Back 276

-contain cerebral spinal fluid

-third ventricle sits between large, lateral ventricles

-fourth ventricle sits behind cerebellum

-lined by choroid plexus

Front 277

Choroid Plexus

Back 277

-lines ventricles

-secretes CSF

-rate: 500mL/day, replenishes 3x/day

Front 278

Cerebrospinal Fluid

Back 278

-produced by choroid plexus in ventricles (mainly lateral)

-sterile, colourless acellular fluid containing glucose

-supports/cushions CNS (floating brain)

-provides nourishment to brain

-removes metabolic waste (arachnoid villi)

-passive flow through ventricles

Front 279

CSF Circulation

Back 279

-produced by ventricles

-flows into third ventricle through Foramen of Monro

-through cerebral aqueduct to fourth ventricle

-enters central canal

-enters subarachnoid space

-flows through foramens of Lushka/Magendie into subarachnoid space

-arachnoid villi absorb CSF and take it out of brain

Front 280

Subarachnoid space

Back 280

-space surrounding CNS, brain and spinal cord

-between arachnoid membrane and pia mater

-comprised of trabeculae structures

-filled with CSF

Front 281

Hydrocephalus

Back 281

-outflow of CSF is blocked

-pressure builds up

-compression of brain blood vessels leads to inadequate blood flow to neurons

-can lead to neuronal damage, cognitive dysfunction

-communicating: arachnoid villi are not absorbing or a block in subarachnoid space

-non-communicating: block between ventricles, CSF buildup in ventricles

Front 282

3 Meninges of CNS

Back 282

-membranes that cover brain/spinal cord

-include subarachnoid space

First Layer: dura mater

-thick, leathery covering below bone

Second Layer: arachnoid membrane

-thinner

Third: Pia Mater

-stuck to brain tissue itself (gray matter)

at top of midline dura forms sinus

Front 283

Dural (Venous) Sinus

Back 283

-CSF returns to blood at dural sinus

-CSF enters dural sinus via arachnoid villi

Front 284

Blood Supply to Brain

Back 284

-glucose is only substrate metabolized by brain (little glycogen)

-brain requires continuous supply of glucose and oxygen

-brain receives 15% of total blood

-few seconds of blood supply interruption can lead to loss of consciousness and later neuronal death

-body will protect glucose supply to brain by breaking down other tissues during starvation

1. Blood pumped from heart.

2. Aorta

3. Common carotid artery

4. Diverges into external carotid (outside of head) and internal carotid (base of brain)

5. Vertebral arteries merge to form basilar artery

5. All arteries form circle of Willis (safety factor, blood can be shunted across)

Front 285

Blood-Brain Barrier

Back 285

-capillary wall lined w/ endothelial cells

-tight junctions

-molecules must diffuse across membrane (lipid soluble)

-glucose and amino acids are actively transported across

-plasma proteins/large molecules can not cross

-ions have difficulty

-ex. lipid soluble drugs (caffeine, alcohol, nicotine)

Front 286

Blood-CSF Barrier

Back 286

-in choroid plexus

-brain can regulate what enters ECF

Front 287

Law of Specific Nerve Energies

Back 287

-regardless of how a sensory receptor is activated the sensation felt corresponds to that of which the receptor is specialized

ex. rubbing eyes in dark room and seeing flashes of light

Front 288

Law of Projection

Back 288

-regardless of where in the brain you stimulate a sensory pathway the sensation is always felt at the sensory receptors location

ex. stimulating somatic sensory cortex and perceiving a somatic sensation in body

ex. phantom limb pain

Front 289

Transduction

Back 289

-opening/closing of ion channels to percieve stimulus energy

Front 290

Slowly Adapting Afferent Response

Back 290

-stimulus is constant

-frequency of action potentials change

-encodes stimulus intensity and moderate stimulus changes

Front 291

Rapidly Adapting Afferent Response

Back 291

-encodes fast stimulus changes

Front 292

Non-Adapting Afferent Response

Back 292

-afferents fire at constant rate

-minority

-encodes stimulus intensity and slow changes

Front 293

Receptive Field

Back 293

-region in space that activates sensory receptor/neuron (afferent)

-graded afferent response across RF

-overlapping RFs produce a population code (brain can pinpoint stimulus)

Front 294

Acuity

Back 294

-ability to differentiate one stimulus from another

-varies depending on RF size (small RF = higher acuity, large RF = lower acuity)

Front 295

Lateral Inhibition

Back 295

-sharpens sensory acuity

-afferents stimulate secondary interneurons that inhibit "next-door" neurons

Front 296

Presynaptic Inhibition

Back 296

-sensory information coming from brain is regulated

-ex. pain tolerance

Front 297

Meissner's Corpuscle

Back 297

-superficial layer somatic receptor

-fluid-filled structure enclosing nerve terminal

-rapidly adapting, light stroking/fluttering

Front 298

Merkel Disk

Back 298

-small epithelial cells around nerve terminal

-superficial layer somatic receptor

-slowly adapting, pressure and texture

Front 299

Pacinian Corpuscle

Back 299

-deep layer receptors (require larger stimulus)

-large concentric capsules and CT surrounding nerve terminals

-rapidly adapting, strong vibrations

Front 300

Ruffini Endings

Back 300

-deep layer receptor

-nerve endings wrap around spindle-like structure

-slowly adapting, stretching/bending of skin

Front 301

Mechanoreceptors

Back 301

-nerve terminals surrounding afferents

-cytoskeletal strands pull open ion channels

-transduction

Front 302

Nociceptors (Pain Receptors)

Back 302

-free nerve endings containing ion channels that open in response to intense mechanical deformation, excess temperature/chemicals

-pain highly modulated (enhanced and supressed)

-visceral pain receptors: activated by inflammation

Front 303

Hyperalgesia

Back 303

-increased enhancement of sensitivity that lasts for days

Front 304

Dorsal Column Pathway

Back 304

-carries ipsilateral touch and proprioception information

-collection of axons going up spinal cord in dorsal portion of white matter

1. Stimulus applied. Afferent propagates through axon.

2. Reaches spinal cord and goes through dorsal root.

3. Does U turn in dorsal column towards brain

4. Synapses on second order neuron in medulla.

5. Axons sent across midline up to medial lemniscus.

6. Axons travel from medulla to thalamus to somatosensory cortex

Front 305

Medulla Lemniscus Pathway

Back 305

-carries contralateral touch and proprioception

Front 306

Anterolateral Pathway

Back 306

-carries controlateral temperature and pain

-axon tract in white matter

1. Nociceptors are activated. Afferents sent.

2. To dorsal horn in gray matter.

3. Contralateral pain/temperature sent up anterloateral column to reticular formation

4. Relays to thalamus and then to somatosensory cortex.

Front 307

Somatosensory Cortex

Back 307

-receives all somatosensory information

-sits behind central sulcus

Front 308

Referred Pain

Back 308

-visceral and somatic afferents commonly synapse on same neurons in spinal cord

-afferents carrying pain information from two different regions (inside/outside body) share secondary neuron

-brain assigns location of pain (usually to somatic sensory region)

-ex. heart attack causes pain in left arm

Front 309

Analgesia

Back 309

selective suppression of pain without effects on consciousness or other sensations

Front 310

Transcutaneous Electrical Nerve Stimulation

Back 310

-painful site/nerves leading from it are stimulated by electrodes on surface of skin

-stimulation of non-pain low threshold afferent fibers leads to inhibition of neurons in pain pathways

-low tech: rub head at site of painful bump

Front 311

Myopic Eyesight

Back 311

-nearsightedness

-eyeball is too long

-too much light refracted in cornea/lens

-cannot see far objects

-correction: concave lens glasses

Front 312

Hyperopic Eyesight

Back 312

-farsightedness

-eyeball is too short

-not enough light is refracted in cornea/lens

-cannot focus near objects

-correction: convex lens glasses

Front 313

Astigmatism

Back 313

-lens or cornea is not spherical

Front 314

Presbyopia

Back 314

-lens becomes stiff

-unable to accommodate for near vision

Front 315

Cataract

Back 315

-changes in lens colour (more opaque)

Front 316

Glaucoma

Back 316

-major cause of irreversible blindness

-aqueous humour forms faster than it can be drained

-retinal cells are damaged due to increased pressure within eye

Front 317

Phototransduction

Back 317

1. Light causes photoreceptors to hyperpolarize

2. Activation of opsin molecule (ex. rhodopsin)

3. G-protein cascade

4. cGMP to GMP

5. Channels close

Front 318

Rods

Back 318

-high sensitivity, night vision

-more rhodopsin (captures more light)

-high amplification (one photon closes many Na+ channels)

-slow response time

-more sensitivity to scattered light

System:

-low acuity

-not present in central fovea

-achromatic

Front 319

Cones

Back 319

-low sensitivity, day vision

-less opsin

-lower amplification

-faster response time

-most sensitive to direct axial rays

System:

-high acuity

-concentrated in fovea

-chromatic

Front 320

Dark Adaptation

Back 320

-bright light to dark

-rods are saturated, cones active in bright light

-temporary blindness until rods take over

-10-15 minutes

-rods inactivated by bright light (no opsin-chromophore molecules in bright light--photons break them apart)

-takes time for opsin and chromophore to reattach

Front 321

Light Adaptation

Back 321

-dark to bright light

-cones are inactive, rods active

-temporary blindness until cones take over

-when rods are active all opsin-chromophore molecules are intact

-cones become saturated very quickly in bright light

-temporary blindness is very brief

Front 322

Retinal Ganglion Cells

Back 322

-axons of retina ganglion cells make up optic nerve

-report relative intensity of light

-intensity of light is perceived as relative to surrounding objects' brightness

-retinal ganglion cells have centre-surround receptive fields

-ganglion cells tell brain how much light is in centre of RF and how much is outside the centre

-some have excitatory centres and inhibitory surround and vice versa

-the more the ganglion cell is firing the more the visual input matches the ganglion cell's preference

Front 323

Colour Vision

Back 323

-photoreceptors sensitive to wavelengths

-opsin molecule determines sensitivity of photoreceptor

-perception of colour is context dependent

-colour vision begins w/ activation of photopigments in cone cells

-L/red cones

-M/green cones

-S/blue cones

Front 324

Colour Blindness

Back 324

-one or more cones are not functioning properly

-genetic defect in opsin molecules

-predominant in males

Front 325

Flow of Visual Information in Brain

Back 325

-visual info leaves retina via optic nerve to brain

-contralateral system

-one retina sees both sides of visual field

-optic chiasm: where two optic nerves come together (some axons cross midline)

-optic tract: contains info from both eyes w/ contralateral field vision

-lateral geniculate nucleus: info travels from optic tract where retinal ganglion axons synapse in thalamus

-optic radiation: info travels from lateral geniculate nerves

-info synapses in visual cortex in occipital lob (both eyes w/ contralateral visual field)

Front 326

Anatomy of Visual Field Deficits

Back 326

1. Lesion in optic nerve: loss of vision in ipsilateral eye

2. Lesion in optic tract: bilateral loss of vision in contralateral visual field

3. Lesion in optic chiasm: bilateral loss of temporal visual hemifields

4. Lesion in primary visual cortex: loss of vision in contralateral visual field

Front 327

Primary Visual Cortex

Back 327

-not sure how recognition process/cortical representation of visual world works exactly

-small RFs

-simple image features

Front 328

Parietal Visual Stream

Back 328

-"where" pathway

-large RFs (spatial features and motion)

-neurons respond to complex information

-info travels to polymodal region of parietal cortex (sensory/visual modalities combine)

Front 329

Temporal Visual Stream

Back 329

-"what" pathway

-large RFs

-complex image features

-optic recognition located in temporal visual cortex

Front 330

Damage Threshold (Hearing)

Back 330

-transection processes in ear can be damaged by loud sounds

-damage threhold less than pain threshold

Front 331

Anatomy of Ear

Back 331

-pinna: specific shape reflects certain frequencies of sound coming from certain locations into external auditory canal

-tympanic membrane at end of external auditory canal

-middle ear: cavity behind tympanic membrane (malleus, incus, stapes: smallest bones in body)

-middle ear connected to back of throat via eustachian tube

-inside bone of skull is inner ear

Front 332

Anatomy of Inner Ear

Back 332

-cochlea: coiled structure where auditory transduction occurs (sensory epithelia)

-semicircular canals are part of vestibular system

Front 333

Flow of Sound Energy

Back 333

1. Pressure waves activate transduction process

2. Pressure waves push/pull ear drum back and forth

3. Tympanic membrane attached to malleus, incus and stapes which couple the ear drum to the oval window.

4. Pressure waves travel through oval window down cochlea around helicotrema and back to round window via scala tympani

5. Flexible basilar membrane that surrounds cochlear duct vibrates up and down as pressure waves travel down duct

Front 334

Motion of Basilar Membrane

Back 334

-frequency dependent

-low frequency: vibrations near helicotrema

-high frequency: vibrations closer to oval/round window

-motion converted into neuronal activity at organ of Corti (w/ inner hair cells/stereocilia)

Front 335

Auditory Transduction

Back 335

1. Tip links connecting each short stereocilia to long sterocilia have mechanically gated channels behind them.

2. During motion the tip links are stretched, opening the mechanoreceptors.

3. K+ enters mechanically gated ion channels

4. Cochlea has lots of extracellular K+

5. Hair cells release neurotransmitter to afferent neurons

6. Stereocilia are pushed closer together and ion channels close. Cell hyperpolarizes and neurotransmission stops.

Front 336

Central Auditory Pathways

Back 336

-8th cranial nerve carries vestibular and auditory information

-up through medulla, diverges as it travels to midbrain/thalamus to two primary auditory cortexes

-information from one ear is represented in both auditory cortexes on either side of midbrain (bilateral representation)

Front 337

Cochlear Implant

Back 337

-implanted through round window

-electrode in scala tympani

-electrodes placed along cochlear spiral to stimulate groups of afferent fibers to respond to different frequencies

Front 338

Vestibular Organs

Back 338

-part of inner ear

-semicircular canals

-utricle: linear ho. acceleration

-saccule: linear vert. acceleration

-mediated by hair cells

Front 339

Vestibular Ocular Reflex

Back 339

-sense of gravity, acceleration, rotational acceleration

-compensates for motion of head

-eyes rotate in opposite direction of head (gaze does not change)

Front 340

Concussion

Back 340

-bleed inside brain

-brain becomes squished due to intracranial pressure

-brainstem containing vestibular ocular reflexes and reflexes for pupils is squished first

-pupils will not dilate

Front 341

Organization of Semicircular Canals

Back 341

-ampula: bulge containing hair cells

-hair cells stick stereocilia into cupula

-semicircular canals are fluid-filled

-rotation of head bends stereocilia due to inertia of fluid inside canals

-triggers transduction

Front 342

Utricle and Saccule

Back 342

-sense of ho./vert. acceleration

-hair cells embedded w/in basal portion of organs

-fluid on top

-stereocilia inserted into mass of jello above

-otoliths: little "rocks" floating above hair cells

-during motion otoliths lag behind (inertia)

-stereocilia bend

-transduction

Front 343

Gustatory System

Back 343

-tase

-chemoreceptors

-taste buds line papillae

Front 344

Taste Transduction

Back 344

-salty: Na+ flows through ion channels, activating afferents

-sour: highly acidic concentration, blocks/interferes w/ channels

-bitter: block ion channels or can activate chemoreceptors that trigger G-protein cascades

-sugars: glucose activates chemoreceptors, G-protein cascade

-umami: glutamate receptors, G-protein cascade

Front 345

Central Taste Pathways

Back 345

-cranial nerves lead from taste buds carrying afferents to medulla

-run through thalamus to ipsilateral gustatory

Front 346

Olfactory System

Back 346

-sense of smell

-chemical stimulus/chemoreceptors

-lining of nasal cavity: olfactory epithelium w/ cilia and mucus

1. mucus traps/dissolves particles

2. dissolved particles bind to olfactory receptor cells

3. Afferent travels down olfactory nerves

Front 347

Olfactory Signal Transduction

Back 347

1. Molecules bind to cilia of receptors

2. Triggers G protein cascade

Front 348

Central Olfactory Pathways

Back 348

-info sent from olfactory receptors to olfactory bulb across skull

-sent to brain via olfactory tract

-projects to limbic system (some odours trigger memories)

Front 349

Conciousness

Back 349

-state of consciousness: level of arousal measured by brain activity and behaviour

-conscious experience: thoughts, feelings, desires, ideas, etc

Front 350

Electroencephalograph (EEG)

Back 350

-measures activity of neurons located near scalp in gray matter of crotex

-frequency is related to levels of responsiveness

-amplitude is related to synchronous neural activity

-alpha rhythms: relaxed w/ eyes closed (low frequency)

-beta rhythms: alert (high frequencies)

Front 351

Stages of Sleep

Back 351

Awake: low ampitude, high frequency EEG

NREM (slow wave) sleep: four stages, increasing amplitude decreasing frequency (30-45 minutes)

REM (paradoxical) sleep: low amplitude, high frequency EEG, resembles awake state (dreaming)

-increased eye movement

-sleep paralysis

Front 352

Sleep Apnea

Back 352

-sudden reduction in respiration during sleep

Front 353

Circadian Rhythm

Back 353

-sleep/wake cycle (~24hrs)

-amount of sleep varies between individual

-regulated by reticular activating system

AWAKE

-increase in norepinephrine/serotonin, aminergic neurons active

-decrease in ACh

-decrease in GABA

-increase in histamine

-increased activation of thalamus/cortex

SLEEP

-decrease in norepinephrine/serotonin

-increase in ACh, cholinergic neurons active

-increase in GABA

-decrease in histamine

-decreased activation of thalamus/cortex

Front 354

Motivation and Emotion

Back 354

-motivation: produces goal directed behaiviour

-emotions: accompany conscious experiences, the way you store sensory inputs

Front 355

Mesolimbic Dopamine Pathway

Back 355

-reward pathway (motivation)

-locus ceruleus in reticular activating system

-dopamine is primary neurotransmitter

-to midbrain then to prefrontal cortex

Front 356

Limbic System

Back 356

-emotions

-amygdala: where emotional scoring of experiences arises

-sits closet o hippocampus (memory)

-olfactory bulb projects to amygdala and hippocampus

Front 357

Altered States of Conciousness

Back 357

-schizophrenia:

-diverse set of problems in basic cognitive processing

-hallucinations/delusions

-reducing affects on dopamine can improve systems

-depression:

-decreased activity in anterior limbic system

-treatment: increase levels of serotonin and norepinephrine in extracellular space around synapses

-bipolar:

-swings between mania and depression

-treatments: lithium can reduce certain synaptic signaling pathways

Front 358

Learning and Memory

Back 358

-declarative memory: conscious experiences that can be put into words

-short term: hippocampus/temporal lobe structures

-long term: various areas of association cortex

procedural memory: skilled behaviour

-short term: widely distributed

-long term: basal nuclei, cerebellum, premotor cortex

consolidation: memories in short term are held and transferred to long term (sleep?)

Front 359

Language

Back 359

-Broca's area: articulation

-Wernicke's area: comprehension

-aphasia: language deficit

Front 360

Sensory Neglect

Back 360

-damage to association areas of parietal cortex causes injured person to neglect parts of body/parts of visual field as though they do not exist

Front 361

Coma/Brain Death

Back 361

coma: extreme decrease in mental functions due to structural, physiological or metabolic impairment of brain

persistent vegetative state: sleep wake cycles are present even though patient is unaware of surroundings

brain death; occurs when brain is no longer functioning/has no possibility of functioning again

Front 362

Selective Attention

Back 362

-avoiding distraction of irrelevant stimuli while seeking/focusing on stimuli more important

-voluntary and reflex mechanisms

Front 363

Preattentive Processing

Back 363

-directs attention to part of sensory world that is of interest and prepares brain's perceptual processes for it

Front 364

Habituation

Back 364

-repeated stimulus, behaviour response adapts

Front 365

Motor Behaviour

Back 365

-purposeful or goal directed

-voluntary and reflexive

Front 366

Muscle control

Back 366

-extension:

-extensor muscle contracts

-flexor muscle relaxes

-increased angle around joint

-flexion:

-flexor muscle contracts

-extensor muscle relaxes

-decreased angle around joint

-limb position maintained by balance of flexor/extensor muscle tension

Front 367

Motor Neurons

Back 367

-only excitatory (ACh)

-alpha: innervate skeletal muscles (extrafusal)

-gamma: innervate muscle spindle (intrafusal)

-cell bodies located in ventral horn of spinal cord or brain stem

-most inputs received from interneurons

Front 368

Polysynaptic Spinal Pathways

Back 368

-incoming through dorsal root ganglion

-ascending sensory information (touch/proprioception)

-branches in sensory afferent go into spinal cord circuitry

-activate interneurons

-interneurons activate motor neurons to send motor efferent through ventral rootss

Front 369

Spinal Interneurons

Back 369

-receives various information (excitatory/inhibitory) and innervates motor neurons

-brain provides a lot of inhibition to spinal cord (ex. inhibition removed, chicken w/ head cut off still runs around)

Front 370

Withdrawal Reflex

Back 370

-polysynaptic

1. Nociceptors activated by tissue damage. Pain afferent sent to spinal cord via dorsal root.

2. Synapses on secondary neuron, crosses midline. Travels to brain via anterolateral column.

3. Branches from nociceptors that synapse w/ interneurons innervate motor neurons. Involuntary movement away from pain stimulus

4. Excitation of motor neurons innervating ipsilator flexor. Inhibition of motor neurons innervating ipsilateral extensor.

Front 371

Stretch Reflex

Back 371

-monosynaptic

-pull muscle, muscle pulls back

-ex. knee jerk

1. Tapping hammer on knee stretches extensor muscle in leg

2. Activation of stretch receptor (touch/proprioception)

3. Afferent travels through dorsal root/dorsal column (ipsilateral)

4. Branches off in gray matter and synapses directly w/ motor neurons.

5. Excitation of motor neurons innervating ipsilateral extensor.

6. muscle contracts to "pull back" muscle and maintain length

7. Inhibition of motor neurons innervating ipsilateral flexor

8. Leg jerks out

Front 372

Inverse Stretch Reflex

Back 372

-controls muscle tension

-muscles can exert too much force

-Golgi tendon organ responds to tension in series w/ muscle

-higher action potentials in contracted muscle than passively stretched muscle

Front 373

Cross Extensor Reflex

Back 373

-contralateral response to withdrawal reflex

-opposite contraction/inhibition of motor neurons on opposite side

-ex. balancing on one leg after pulling foot off nail

Front 374

Muscle Spindle

Back 374

-proprioceptive somatosensory organ

-parallel w/ extrafusal muscle

-stretch receptors that measure muscle length

-intrafusal muscle fibers on either side of stretch receptors (activated by gamma motor neurons)

-reports muscle length

-1a primary afferent detects changes in muscle length and some static length

-II secondary detects static length

-intrafusal fibers maintain muscle spindle sensitivity (alpha-gamma coactivation)

Front 375

Golgi Tendon Organ

Back 375

-in series w/ extrafusal muscle

-inside tendons

-feels force extrafusal muscle is generating

-free nerve endings w/ mechanically gated ion receptors

-1b afferents: touch/proprioception

-collagen fibers surround nerve endings

-collagen fibers pinch nerve endings, opening mechanoreceptors during conctraction

Front 376

Ia and II Afferents

Back 376

Ia Primary: rapidly adapting

-activated mostly during change in muscle length

-nuclear bag fibers

II Secondary: signals static muscle length

-nuclear chain fibers

Front 377

Alpha-Gamma Coactivation

Back 377

-prevents sensitivity loss in muscle spindles

-extrafusal muscle fibers activated by alpha motor neurons (muscle shortens)

-gamma motor neurons activate intrafusal muscle fibers (pull muscle spindle out)

-prevents muscle spindle from collapsing (cuz it gets floppy)

Front 378

Motor Control Organization

Back 378

Middle level: executes individual muscle contractions

-corrections based on sensory info

-becomes involuntary over time

Front 379

Corticospinal Pathway

Back 379

-from primary motor cortex to brainstem/spinal cord

-axons cross medulla in brainstem

-continue down white matter tract of spinal cord

-innervate appropriate interneurons as well as directly innervate motor neurons

-axons sent to skeletal muscles

-controlateral control

-skilled movments

Front 380

Extrapyramidal Pathway

Back 380

-axons travel down white matter of spinal cord (originates in brainstem)

-only innervate interneurons

-ipsilateral and contralateral control

-trunk/posture

Front 381

Voluntary Control of Movement

Back 381

-conscious initiation of movement in frontal cortex

-activity move to premoter cortex

-finally to primary motor cortex

-sends efferents

Front 382

Muscle Tone

Back 382

-resistance of skeletal muscle to stretch

-descending pathways (corticospinal/extrapyramidal) produce level of inhibition in spinal cord

Front 383

Hypertonia

Back 383

-damage to descending motor pathway

-abnormallly high muscle tone

Front 384

Spasticity

Back 384

-damage to descending motor pathway

-overactive motor reflexes

Front 385

Hypotonia

Back 385

-damage to motor neurons

-abnormally low muscle tone

Front 386

Atrophy

Back 386

-damage to motor neurons

-loss of muscle mass

Front 387

Middle Layers of Motor Control

Back 387

-basal nuclei

-cerebellum

-help determine sequence of movements to accomplish desired action without having to think about it

Front 388

Basal Nuclei

Back 388

-ganglia

-white matter

Front 389

Parkinson's

Back 389

-basal nuclei disorder

-reduced dopamine input to basal nuclei

-akinesia: reduced movements

-bradykinesia: slow movements

-muscular rigidity

-resting tremor

Front 390

Huntington's

Back 390

-genetic mutation that causes widespread loss of neurons in brain

-manifests later in life

-neurons in basal nuclei are preferentially lost

-hyperkinetic disorder: excessive motor movements

-choreiform movements: involuntary random, jerky movements of limbs/face

Front 391

Deep Brain Stimulation

Back 391

-treatment for Parkinson's

-electrodes deep in parts of basal nuclei

-activates them by electrical impulses

Front 392

Cerebellum

Back 392

-receives sensory information

-contains almost half brain's neurons

-makes corrections (coordination)

-w/out a cerebellum you have poor coordination

Front 393

Asynergia

Back 393

-smooth movements are divided into separate components

-have to think about individual contractions

Front 394

Dysmetria

Back 394

-unable to target movements correctly "past pointing"

Front 395

Ataxia

Back 395

incoordination of muscle groups (awkward gate)

Front 396

Intention Tremor

Back 396

during voluntary movements

Front 397

Pain Inhibition

Back 397

-descending pathways regulate nociceptive information

-periaqueductal gray matter in midbrain

-reticular formation in medulla

-dorsolateral funiculus

-under stress you often don't notice you've been injured until later

-allows you to gtfo