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South College Human Physiology > Week 2- Nerve and Muscle Physiology > Flashcards

Week 2- Nerve and Muscle Physiology Flashcards

1
Q

Diffusion potential

A

A potential difference generated across a membrane by ions flowing down their concentration gradient

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2
Q

Role of permeability in creating diffusion potential

A

The membrane has to be permeable to that ion

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3
Q

What determines the size of the diffusion potential?

A

The size of the concentration gradient

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4
Q

Equilibrium potential

A
  • A diffusion potential
  • The potential difference across the membrane when ions have reached equilibrium (no net diffusion)
  • Chemical and electric driving forces are equal and opposite
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5
Q

What equation calculates the equilibrium potential

A

Nernst equation

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6
Q

Potassium accumulates where?

A

Inside the cell

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7
Q

Sodium accumulates where?

A

Outside the cell

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8
Q

Membrane potential

A

Difference in electrical charge across a membrane

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9
Q

What can cause the membrane potential?

A
  • Passive ion diffusion (ex: open Na+ channel)

- Electrogenic pumping (ex: Na+/K+ ATPase)

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10
Q

Is the cell membrane more permeable to Na+ or K+

A

AT REST, K+; there are K+ leak channels

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11
Q

How is equilibrium different than having the same chemical concentration?

A

Equilibrium takes into account the electrical charges present and their effects on flow as well as the chemical concentration of ions

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12
Q

Why is resting membrane potential (Vm) so close to E(K)?

A

The membrane is more permeable to K+ than to Na+

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13
Q

Why is the cell membrane more permeable to K+ than Na+

A
  • Na+/K+ pump

- K+ leak channels

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14
Q

What would a saline solution of KCl do to membrane potential?

A

It takes away the membrane potential, and when this happens to the heart or diaphragm, no action potential can take place, killing the person.

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15
Q

Depolarization

A

Potential becomes less negative

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16
Q

Hyperpolarizationn

A

Potential becomes more negative than resting membrane potential

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17
Q

Overshoot

A

More positive than 0 mV

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18
Q

Repolarization

A

Potential moves toward resting membrane potential (more negative)

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19
Q

Excitability

A

The potential can change from resting membrane potential, can depolarize and repolarize

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20
Q

Threshold

A

The potential at which an action potential will always happen

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21
Q

Action potential

A

Regenerating depolarization that propagates along an excitable membrane

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22
Q

Propagate

A

Conducts without getting weaker

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23
Q

Excitable

A

Capable of generating an action potential

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24
Q

How fast are action potentials?

A

~60 m/s

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25
Q

Basic characteristics of an action potential

A
  • All-or-nothing
  • Constant amplitude
  • Starts w/ depolarization
  • Involves change in permeability
  • Relies on voltage-gated channels
  • Constant conduction velocity
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26
Q

All-or-nothing

A

Action potential will not happen unless depolarization reaches a threshold voltage (~15 mV positive to resting)

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27
Q

Constant amplitude

A
  • APs are not additive

- Info depends on frequency

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28
Q

Starts w/ depolarization

A

Requires a stimulus for depolarization

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29
Q

Involves change in permeability

A

Na+ flows into the cell

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30
Q

Relies on voltage-gated channels

A

Determines which ions can come in and out of the cell

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31
Q

Constant conduction velocity

A
  • True for any given fiber, but not across all fibers

- Larger diameter => faster

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32
Q

Velocity for myelinated fibers

A

V (m/s) = fiber diameter (mm) x 4.5

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33
Q

Velocity for unmyelinated fibers

A

V (m/s) = square root of fiber diameter

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34
Q

At rest, which gates are open for Na+ voltage gated channels?

A
  • Activation gate = closed

- Inactivation gate = open

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35
Q

What happens to the Na+ activation gates after action potential occurs?

A
  • Activation gate opens

- Same stimulus closes inactivation gate, but this happens more slowly

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36
Q

What happens to the K+ activation gates after action potential occurs?

A
  • Starts closed

- Opens slowly

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37
Q

What happens during the upstroke of the action potential?

A
  • Na+ permeability increases

- Happens because Na+ channels open

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38
Q

What happens during the downstroke of the action potential?

A
  • Na+ permeability decreases

- K+ permeability increases (K+ channels open)

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39
Q

How do nerves prevent action potentials from propagating backwards?

A

Inactivation gates and refractory periods

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40
Q

Myelinationn

A

Axons are surrounded by a myelin sheath

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41
Q

What cells are responsible for myelination?

A

Schwann cells

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42
Q

Node of Ranvier

A

A break in the myelin occurring every 1-3 mm

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43
Q

Saltatory Conduction

A

Current travels faster under the myelin, and is amplified at the nodes of Ranvier

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44
Q

Multiple sclerosis

A

Auto-immune disease where in nerves of the CNS demyelinate

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45
Q

Main classes of muscle cells

A
  • Skeletal muscle
  • Cardiac muscle
  • Smooth muscle
  • Myoepithelial cells
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46
Q

Muscle organizational hierarchy

A

Muscle –> Fasciculus –> Fibers –> Myofibrils –> Sarcomeres –> Myofilaments

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47
Q

Epimysium

A

Connective tissue that surrounds the entire muscle

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48
Q

Perimysium

A

Connective tissue that surrounds each fasciculus

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49
Q

Endomysium

A

Connective tissue that surrounds each muscle fiber

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50
Q

Where are blood vessels and nerves that supply muscles located?

A

In the perimysium

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51
Q

Sarcomere

A

Portion of the myofibril between 2 adjacent Z disks

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52
Q

Light Bands

A
  • I band

- Only actin

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53
Q

Dark Bands

A
  • A band

- Actin and myosin overlapping

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54
Q

Where is actin found outside of the muscle?

A
  • Cytoskeleton of the cell
  • Determines shape of the cell’s surface
  • Important for whole cell locomotion
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55
Q

Alpha-actinin

A
  • Contractile bundle

- Loose packing allows myosin-II to enter the bundle, permitting contraction

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56
Q

Fimbrin

A
  • Parallel bundle

- Tight packing prevents myosin-II from entering the bundle, making contraction impossible

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57
Q

Myosin-II

A
  • Part of a superfamily of myosin proteins
  • Myosin superfamily is part of a larger family of motor proteins
  • Skeletal muscle myosin was the first motor protein identified
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58
Q

If myosin-II was the first motor protein identified, why is it called “myosin-II”?

A

It has two heads

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59
Q

Composition of myosin

A
  • 2 heavy chains (in the tail)

- 4 light chains (part of the head)

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60
Q

How many individual myosin molecules make up the myosin myofilament?

A

200+

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61
Q

What are the protruding heads of myosin called?

A

Cross-bridges

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62
Q

Titin

A

Spring-like protein that connects myosin with z-line

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63
Q

Troponin

A

Binding site for calcium in skeletal muscle

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64
Q

Tropomyosin

A
  • Wraps around actin

- Stabilizes the thin filament

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65
Q

Tropomodulin

A

Caps actin closer to the M line

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66
Q

Cap Z

A

Caps actin at the Z disc in conjunction with alpha-actinin

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67
Q

Does the length of the muscle filaments change during muscle contraction?

A

No

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68
Q

How often does the myosin head cycle during a muscle contraction?

A

~5x/second

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69
Q

Nebulin

A
  • Molecular ruler

- Helps determine the exact length of each actin filament

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70
Q

Steps of the Walk-Along Theory of Contraction

A
  • Attached
  • Released
  • Cocked
  • Force-generating
  • Attached
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71
Q

Attached

A
  • Start of the cycle
  • Myosin head is attached to actin
  • ATP absent
  • Short-lived phase during active contraction
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72
Q

Released

A
  • ATP binds to myosin head

- This allows myosin to detach from actin

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73
Q

Cocked

A
  • Head moves along the actin filament

- ATP hydrolysis, ADP and P(i) stay bound to myosin head

74
Q

Force-generating

A
  • Weak binding causes release of P(i)
  • Tight binding occurs at the same time
  • POWER STROKE
  • ADP is lost during power stroke, returning to start of cycle
75
Q

Parts of troponin complex

A
  • Troponin I
  • Troponin C
  • Troponin T
76
Q

Troponin I

A

Inhibits binding of myosin head

77
Q

Troponin C

A
  • Binds to calcium

- Causes tropomyosin to move out of the way, making room for myosin heads

78
Q

Troponin T

A

Binds to tropomyosin

79
Q

Types of synapses

A
  • Electrical

- Chemical

80
Q

Electric Synapse

A

Allows current to flow from one excitable cell to another via gap junctions

81
Q

How high is resistance in gap junctions?

A

Low

82
Q

Where are electrical synapses found?

A

Cardiac muscle and some types of smooth muscles

83
Q

Directionality of electric synapses

A

Bidirectional

84
Q

Synaptic delay in electric synapses?

A

No synaptic delay

85
Q

Chemical Synapse

A

There is a gap b/t the presynaptic membrane and post synaptic membrane

86
Q

What is the gap between the pre- and postsynaptic membrane called?

A

synaptic cleft

87
Q

How is information transmitted b/t the pre- and postsynaptic cleft?

A

Via neurotransmitters

88
Q

What two effects can the potential have in a chemical synapse?

A
  • Excitatory

- Inhibitory

89
Q

Directionality of chemical synapses

A

Unidirectional

90
Q

Synaptic delay in chemical synapses?

A

There is a synaptic delay

91
Q

Neuromuscular Junction

A

Connection b/t nerve and muscle fiber

92
Q

Motor End Plate

A

Part of the muscle fiber in direct contact with the nerve

93
Q

Why are there invaginations in the motor end plate?

A

To increase surface area for neurotransmitters to diffuse

94
Q

What are the receptors for ACh called?

A

Nicotinic receptors

95
Q

What happens when ACh binds to the receptor?

A

Na+ flows into the cell

96
Q

Why do only Na+ ions pass through, when the nicotinic channel is big enough for K+ and Ca2+ as well?

A
  • Only Na+ and K+ have large enough concentration

- Negative potential attracts Na+ influx and prevent K+ efflux

97
Q

End-plate potential

A
  • The local positive potential that occurs when ACh binds to the nicotinic receptor
  • Generates action potential
98
Q

How much can the potential change in the end-plate potential?

A

50-75 mV

99
Q

How much potential change is required for an action potential?

A

20-30 mV

100
Q

What causes the stimulation of the motor end plate to end?

A

Removal of ACh

101
Q

How is ACh removed?

A
  • ACh-esterase enzyme

- Spillover of ACh

102
Q

What is ACh spillover?

A

Some ACh will diffuse out of the synaptic cleft into the interstitial space

103
Q

What enzyme facilitates the formation of ACh?

A
  • Choline acetyltransferase

- Choline + Acetyl CoA – “ase” –> ACh

104
Q

What is the reaction for ACh degradation?

A

ACh – “ase” –> Choline + Acetate

105
Q

Steps of the Neuromuscular Junction

A

1) Nerve impulse arrives, opens voltage-gated Ca2+ channels –> stimulates release of ACh
2) ACh binds to nicotinic receptors on muscle cell, allowing the ACh-gated channel to open, bringing in Na+ (End-plate potential)
3) Influx of Na+ causes local depolarization, opening Na+ voltage-gated channels, causing the action potential
4) Impulse reaches T-tubules, causes dihydropyridine (DHP) receptor to open
5) DHP opening causes the Ca2+ release channel (ryanodine receptor) on SR to open and release Ca2+ –> cross-bridge cycle

106
Q

How is calcium put back into sarcoplasmic reticulum

A

SERCA

107
Q

Excitation-Contraction Coupling

A

Action potential –> myoplasmic [Ca++] goes up –> muscle twitch

108
Q

Steps of Excitation-Contraction in skeletal muscle

A

1) AP in muscle membrane
2a) Depolarization of T-tubules
2b) SR opens and releases Ca++ (DHPR pulls open ryanodine receptors)
3) Intracellular [Ca++] goes up
4) Ca++ binds to tropinin-C
5) Tropomyosin moves, allowing actin and myosin to interact
6) Cross-bridge cycling
7) Ca++ collected by SERCA into SR –> relaxation

109
Q

Agents that alter neuromuscular function

A
  • Botulinum toxin
  • Curare
  • Tetrodotoxin
  • Neostigmine
  • Hemicholinium
110
Q

Botulinum toxin

A
  • Blocks ACh release from nerve terminal

- Causes paralysis and eventually death (respiratory failure)

111
Q

Curare

A
  • Competes w/ ACh for its receptor
  • Max doses cause paralysis and death
  • Therapeutically used for anesthesia
112
Q

Tetrodotoxin

A
  • Japanese puffer fish

- Inhibits Na+ channels

113
Q

Neostigmine

A
  • AChE inhibitor

- Used to treat Myasthania Gravis

114
Q

Hemicholinium

A

Blocks choline reuptake, depleting ACh stores

115
Q

Excitatory Postsynaptic Potential

A

Depolarizes the postsynaptic cell

116
Q

Examples of EPSPs

A
  • ACh
  • Norepinephrine
  • Epinephrine
  • Dopamine
  • Glutamate
  • Serotonin
117
Q

Inhibitory Postsynaptic Potential

A
  • Hyperpolarize postsynaptic cell

- Via opening Cl- or K+ channels

118
Q

Examples of IPSPs

A
  • GABA

- Glycine

119
Q

Length-Tension Relationship

A
  • There is an ideal level of overlap between actin and myosin to maximize tension
  • Too much or too little overlap will lead to less tension
120
Q

What produces passive tension?

A

The cytoskeleton and other connective tissue

121
Q

When does passive tension come into play?

A

Only at longer lengths

122
Q

What is the force-velocity relationship?

A
  • As force goes up, velocity goes down

- As force goes down, velocity goes up

123
Q

How is speed of contraction determined?

A

Vmax of myosin ATPase

124
Q

Characteristics of high Vmax of myosin ATPase

A
  • Stained white
  • Rapid cross-bridge cycling
  • Rapid rate of shortening (fast fiber)
125
Q

Characteristics of low Vmax of myosin ATPase

A
  • Stained red
  • Slow cross-bridge cycling
  • Slow rate of shortening (slow fiber)
126
Q

Fast vs slow twitch fibers in whole muscle

A

Most muscle have both types, with differing proportions

127
Q

Fiber types and motor units

A

All of the fibers in a given motor unit will be the same fiber type (i.e. fast or slow)

128
Q

Characteristics of Slow (Type I) fibers

A
  • Oxidative
  • Small diameter
  • High myoglobin content
  • High capillary density
  • Many mitochondria
  • Low glycolytic enzyme content
129
Q

Characteristics of Fast (Type II) fibers

A
  • Glycolytic
  • Large diameter
  • Low myoglobin content
  • Low capillary density
  • Few mitochondria
  • High glycolytic enzyme content
130
Q

How many fibers are in small motor units?

A

As few as 10 fibers/unit

131
Q

Function of small motor units

A
  • Precise control

- Rapid reacting

132
Q

How many fibers are in large motor units?

A

As many as 1000 fibers/unit

133
Q

Function of large motor units

A
  • Coarse control

- Slower reacting

134
Q

Why do motor units overlap?

A

Provides coordination

135
Q

Size principle

A

Motor units will be recruiting from smallest to largest

136
Q

Force summation

A

Increased contraction intensity as a result of the additive effect of twitch contractions

137
Q

Types of force summation

A
  • Multiple fiber

- Frequency

138
Q

Multiple fiber summation

A
  • Increase in number of motor units contracting at the same time
  • Size principle
139
Q

Frequency summation

A

Increase in the frequency of contraction in a single motor unit

140
Q

Staircase Effect

A
  • Decreasing [Ca++] initiates relaxation
  • If the muscle is stimulated before relaxation completes, the new twitch adds onto the previous one
  • If AP frequency is high enough, the twitches add together until “fused tetanus”
141
Q

Ways muscles remodel and grow

A
  • Hypertrophy
  • Hyperplasia
  • Lengthening
142
Q

Muscle Hypertrophy

A
  • Common
  • Takes weeks
  • Caused by near maximal force development
  • Myofibrils split
  • Increased force generation
143
Q

Muscle Hyperplasia

A
  • Rare
  • Formation of new muscle fibers
  • Can be caused by endurance training
  • Increased force generation
144
Q

Muscle Lengthening

A
  • Occurs with normal growth
  • No change in force development
  • Greater shortening capacity and speed of contraction
145
Q

Muscle Atrophy

A
  • Shrinking of muscle fibers

- Weeks/months

146
Q

Muscle Atrophy w/ fiber loss

A
  • Muscle fibers shrink to the point of disappearing
  • Disuse for months/1-2 years
  • Very difficult to replace lost fibers
147
Q

Causes of atrophy

A
  • Devervation/neuropathy
  • Tenotomy
  • Sedentary lifestyle
  • Plaster cast
  • Space flight (zero gravity)
148
Q

Effects of atrophy on muscle performance

A
  • Degeneration of contractile proteins

- Decrease max force and velocity of contraction

149
Q

Why does smooth muscle lack striations

A
  • Striations come from actin and myosin arranged in sarcomeres
  • Actin and myosin are not arranged in sarcomeres in smooth muscle
150
Q

Smooth muscle functions

A
  • Motility

- Tension

151
Q

Smooth muscle and motility

A
  • Move things through passages

- EX: propel chyme through GI tract

152
Q

Smooth muscle and tension

A

EX: maintain appropriate vascular diameter in blood vessels

153
Q

Types of smooth muscle

A
  • Unitary/Visceral/Single-unit
  • Multiunit
  • Combo
154
Q

How are unitary/visceral/single-unit smooth muscle cells connected?

A

Via gap junctions

155
Q

Where are unitary/visceral/single-unit smooth muscles located?

A
  • GI tract
  • Bladder
  • Uterus
  • Ureter
156
Q

Characteristics of Unitary/Visceral/Single-unit

A
  • Spontaneous pacemaker activity (slow waves)

- Mostly phasic

157
Q

How are multiunit smooth muscles connected?

A

NOT by gap junctions

158
Q

Where are multiunit smooth muscles located?

A
  • Iris
  • Ciliary muscles of the lens
  • Vas deferens
159
Q

Characteristics of multiunit smooth muscles

A
  • Each fiber acts as its own unit
  • Little/no coupling between cells
  • Densely innervated by ANS
  • Mostly tonic
160
Q

Where is combo smooth muscle located?

A

Vascular smooth muscle

161
Q

How does smooth muscle differ from skeletal muscle?

A
  • Has actin and myosin, but no troponin complex

- No striations

162
Q

Dense bodies in smooth muscle

A
  • Serve similar function to Z discs

- Large numbers of actin attached to dense bodies

163
Q

How much can smooth muscle contract vs skeletal muscle?

A

Up to 80% of their length vs 30% in skeletal muscle

164
Q

Myosin ATPase activity in smooth muscle compared to skeletal muscle

A
  • Very reduced

- 1/10 to 1/300 the amount of energy to maintain the same tension

165
Q

Time for contracting and relaxing in smooth muscle vs skeletal muscle

A

Smooth muscle needs more time to contract and relax

166
Q

Maximum force in smooth vs skeletal muscle

A
  • 4-6 kg/cm^2 in smooth muscle

- 3-4 kg/cm^2 in skeletal muscle

167
Q

How does smooth muscle maintain tonic contractions for long periods of time?

A

Uses minimal energy using the latch mechanism

168
Q

Stress relaxation vs reverse stress relaxation in smooth muscle

A

Increases or decreases tension to maintain pressure to accommodate large changes in volume (i.e. blood pressure)

169
Q

Myogenic

A
  • Spontaneously active

- Smooth muscle is myogenic

170
Q

State of the SR in smooth muscle

A

Poorly developed

171
Q

How does excitation-contraction coupling differ in smooth vs skeletal muscle?

A
  • Same actin-myosin interaction

- No troponin complex

172
Q

When does myosin hydrolyze ATP in smooth muscle?

A

When myosin is phosphorylated on the regulatory light chain

173
Q

Myosin light chain kinase

A
  • MLCK

- Phosphorylates the light chain (attaches a phosphate)

174
Q

Myosin light chain phosphatease

A
  • MLCP

- Removes a phosphate

175
Q

How is smooth muscle myosin-based?

A

Skeletal muscle is regulated through actin, but smooth muscle is regulated through myosin

176
Q

How is smooth muscle Ca++ sensitive?

A

MLCK is active only when Ca++ is bound to calmodulin

177
Q

Major points of smooth muscle contraction

A

1) “Stimulus” causes Ca++ to enter the cell (either from ECF or SR)
2) Ca++ binds to calmodulin
3) Ca++/calmodulin/MLCK complex leads to phosphorylation of myosin light chain (requires 1 ATP)
4) MLC is part of the myosin head
5) Phosphorylated myosin head binds to actin leading straight into power stroke (automatic)
6) 2nd ATP is required to release myosin head from actin
7) Cross-bridge cycling requires both MLCK and MLCP
8) MLCP activity can change calcium sensitivity

178
Q

What can stimulate skeletal muscle vs smooth muscle?

A 
Skeletal Muscle
- Nervous system
Smooth Muscle
- Nervous system
- Hormones
- Stretch
- Other chemicals
179
Q

Complexity of smooth muscle neuromuscular junction vs skeletal muscle

A

Less complex and less understood than skeletal muscle

180
Q

Varicosities

A

Bulges terminal axons that contain neurotransmitters

South College Human Physiology (4 decks)

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