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PHA 511 > 1. Nervous System and Muscle Physiology > Flashcards

1. Nervous System and Muscle Physiology Flashcards

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1
Q

Neuron: Regions

A

Cell body (soma)
Dendrites (impulses to cell body)
Axon hillock (initiation of AP)
Axon (impulses away from body)

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2
Q

60-40-20 Rule

A

60% of body weight is water

40% of body weight is ECF

20% of body weigh is ICF

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3
Q

ECF

A

75% interstitial fluid

25% plasma

Separated by capillary wall

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4
Q

Potassium (K)

A

Higher inside cell (ICF)

Circle K

Moves out of cell

Greatest influence on resting membrane potential

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5
Q

Sodium (Na)

A

Higher outside cell (ECF)

Moves into cell

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6
Q

Chloride (Cl)

A

Higher outside cell (ECF)

Moves into cell

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7
Q

The membrane must be more permeable to some ions and less permeable to others

A

Number and opening probabilities of ion channels are key

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8
Q

Primary Active Transport

A

Directly requires ATP

Ex: Na K ATPase

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9
Q

Secondary Active Transport

A

Utilizes ATP indirectly

Ex: Na and glucose movement into cell - relies on gradient created by Na K ATPase

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10
Q

Facilitated Diffusion

A

Passive movement of molecules across membrane with the help of a membrane protein

Ex: glucose

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11
Q

Cell Membrane Transport: Across Membrane

A

Endocytosis (pinocytosis, phagocytosis)

Exocytosis

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12
Q

Cell Membrane Transport: Through Membrane

A

Diffusion
Osmosis
Protein mediated transport (primary active, secondary active, facilitated diffusion)

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13
Q

Simple Diffusion

A

Linear

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14
Q

Protein Mediated Transport

A

Curve with a plateau - exhibits saturation

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15
Q

Membrane Ion Channels

A

Selective

Sometimes open, sometimes closed

  • Voltage operated
  • Receptor (ligand) operated
  • Stretch activated
  • Ungated (open all the time)
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16
Q

Conductance

A

The number of channels that are open in a membrane

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17
Q

Resting Membrane Potential

A

Potential difference that exists across the membrane of excitable cells

Established by diffusion potentials (K concentration gradient)

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18
Q

Diffusion Potentials

A

Depends on:

  • ions present
  • permeability (conductance) of each ion
  • electrochemical gradients of each ion
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19
Q

NaKATPase

A

Electrogenic (transfers positive charge out cell, unequal)

3 Na out, 2 K in

Necessary to create and maintain K concentration gradient - establishes resting membrane potential

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20
Q

Resting Membrane Potential: K

A

K leaves the cell (leaving being negative charge)

Negative charges build up inside membrane - establishing RMP

Inside: -70
Outside: 0

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21
Q

Ion Equilibrium Potentials

A 
Na = +65
K = -85
Cl = -90
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22
Q

Action Potential

A

Involves voltage gated channels (Na)

All or none phenomenon (has a threshold (-50))

Non decremental propagation

  • occurs along axon without decay
  • same strength at beginning and end
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23
Q

Action Potential: Phases

A
  1. upstroke: gNa&raquo_space; K
  2. repolarization: gK>gNa
  3. after hyperpolarization: gK»gNa
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24
Q

During which interval of the action potential would the O2 consumption in milliliters of O2 most exceed the resting level?

A

When the NaK pump reestablishes gradients across the membrane (return to rest) - ATP usage

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25
Myelinated Fibers
Saltatory conduction (node to node) Nodes contain high concentration of voltage gated Na channels Insulation: good for conduction Skipping
26
Unmyelinated Fibers
Electrotonic conduction Low density of voltage gated Na channels spread throughout axon Less efficient/fast Large diameter = faster conduction Walking one foot in front of other
27
Multiple Sclerosis
MRI: gadolinium enhancing brain lesions CSF: oligoclonal IgG bands (Dawson's fingers around periventricular veins - inflammation) Autoimmune disease Loss of myelin from CNS axons - replaced by scar tissue (sclerosis) - Difficulty walking due to demyelinated axons (Loss of current at demyelinated segment - falls below threshold - no AP - weakness) - Deep tendon reflexes working early in disease - Eventual degeneration of nerves will lead to muscle atrophy and weakness
28
Pre-synaptic Neuron
Contains NT
29
Post-synaptic Neuron
Contains R
30
Synaptic Delay
1-5 msec for chemical transmission to occur No physical continuity bt pre and post synaptic neurons
31
Synapse: excitatory c. inhibitory
Depends on type of receptor present - not the NT
32
Amplification
Release of more neurochemical transmitter More NT = more R bound = bigger response
33
Characteristics of Neurotransmitters
Must meet all 4: 1. synthesized in presynaptic cell, enzymes for synthesis must be present in neuron 2. must be released by presynaptic cell with stimulation in sufficient quantity to elicit postsynaptic response 3. Mechanisms for removal or inactivation must exist 4. when applied exogenously, must mimic in vivo response
34
Synaptic Transmission
1. AP at axon terminal 2. voltage gated Ca channels open 3. Ca enters cell 4. Ca signals to vesicles 5. Vesicles move to membrane 6. Docked vesicles release NT - exocytosis 7. NT diffuses across synaptic cleft - binds to receptors
35
Postsynpatic Potentials
EPSP (depolarization) -helps Na and K move IPSP (hyperpolarization) -helps Cl or K move
36
Graded Potentials
Electrotonic conduction Chemical gated channels No refractory period No threshold Amplitude dependent on magnitude of stimulus Exhibits decremental conduction
37
Choline Esters
Small molecule, rapidly acting Acetylcholine Receptors: - nicotinic (excitatory) - muscarininc (inhibitory)
38
Biogenic Amines
Small molecule, rapidly acting ``` Dopamine Epinephrine Histamine Norepinephrine Serotonin ``` Receptors (for epi,norepi) - alpha R - beta R
39
Amino Acids
Small molecule, rapidly acting y aminobutyric acid (GABA) glutamate glycine
40
Neuropeptides
Larger, longer acting ``` Some: ACTH Endorphins Oxytocin Secreting Vasopressin ```
41
Synaptic Transmission at Neuromuscular Junction
1. AP travels down motoneuron to presynaptic terminal 2. Depolarization opens Ca2+ channels 3. ACh released into synaptic cleft (exocytosis, ATP and Ca2+ requiring) 4. ACh R binding at motor end plate 5. Na entry, K efflux via open channel 6. Motor end plate depolarization (EPP) 7. ACh degradation via acetylcholineesterase, choline reuptake via Na/choline symport
42
Myasthenia Gravis
Muscle weakness Endrophonium (tensilon) test: positive Plasma testing: antibodies against ACh R Autoimmune disease Destruction of Ach receptors on motor end plates Normal Ach release Failure does not occur until 70% of Ach R damaged (safety factor)
43
Safety Factor
Measures how much larger EPP is compared to threshold Normally, magnitude of EPP is large - guarantees depolarization to threshold
44
Agents Affecting Neuromuscular Transmission
Botulinum toxin (prevents Ach release) Hemicholinium (blocks Na/choline transporter) Curare (competition for binding on motor end plate) AChE inhibitors (prevents AChE from breaking down ACh)
45
Flaccid Paralysis
Muscles cannot contract Limp, flappy Botulinum toxin
46
Spastic Paralysis
Continuous muscle contraction Rigid
47
AP and the Sarcomere
AP travels inward through sarcomere through T tubules and along surface of muscle fiber
48
Contraction of Skeletal Muscle
A band: no change I band: shortens H zone: shortens Z lines: closer together
49
Excitation Contraction Coupling in Skeletal Muscle
1. AP in muscle membrane 2. Depolarization of T tubules 3. Opens SR Ca2+ release channels 4. Increase intracellular Ca2+ 5. Ca2+ binds troponin C 6. Tropomyosin moves - actin myosin interaction 7. Cross bridge cycling and force generation 8. Ca2+ reaccumulated by SR --> relaxation Continues as long as intracellular Ca is high
50
Muscle Cell At Rest
Cytosolic Ca2+ low Myosin and actin dissociated Myosin head holds ADP, Pi Binding site on actin covered
51
Muscle Cell After Increased Intracellular Ca
Ca2+ binds to troponin C Myosin binding sites uncovered Myosin heads bind to actin Cross bridges formed
52
Cross Bridging Cycle: Power Stroke
Force produced by myosin head pivots ADP and Pi released Bond bt actin and myosin stronger Cross bridges pivot (~45 degrees) Tension produced - "twitch" Contractile force is proportional to number of cross bridges formed
53
Cross Bridging Cycle: Myosin Release
ATP binds to myosin Cross bridges break
54
If ATP supply fails...
cross bridges are maintained -- rigor mortis
55
Cross Bridge Cycle: Regeneration of Activated Myosin
ATP hydrolyzed to ADP and Pi - stay bound Myosin re-energized Myosin displaced toward + end of actin Next cross bridge cycle can occur Cycle repeats as long as Ca is bound to troponin
56
Relaxation
Depends on prompt Ca removal
57
Drop in Cytosolic Ca Levels
Ca dissociates from troponin C Tropomyosin/troponin complex to original conformation Binding site on actin sterically blocked by tropomyosin
58
Sarcomere
Basic contractile unit Delineated by Z disks ``` Thick filaments Thin filaments M line H zone A band I band ```
59
Temporal Sequence of Events in Skeletal Muscle Contraction
1. AP 2. Rise in intracellular Ca 3. Tension
60
Duchenne's Muscular Dystrophy
Poor muscle coordination Weak muscles/grip strength Hypertrophied muscles Plasma analysis: elevated creatine kinase Muscle biopsy Loss of dystrophin
61
Creatine Kinase
Elevated when muscles are damaged
62
Duchenne's Muscular Dystrophy: Dystrophin
Structural link bt cytoskeleton and muscle cell Without: alters transmission of tension - damage to cell membrane (sarcolemma wilts/becomes unstable) - creatine kinase leaks out of cell - muscle weakness
63
Pseudohypertrophy of calf muscles due to inflammatory response
Replacement of damaged muscle cells with scar tissue Calves look okay but really its scar tissue

PHA 511 (7 decks)

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