Nerve and Muscle Flashcards

1
Q

components of CNS

A

cerebral cortex
cerebellum
brainstem
spinal cord

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2
Q

components of PNS

A

peripheral nerves

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3
Q

neurons

A

10% of cells in CNS; 50% of volume
larger than glia
3 types: afferent, efferent, interneurons

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4
Q

glia

A

90% of cells in CNS
provide physical and chemical support to neurons

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5
Q

satellite cells

A

glial cells
provide structure/support isolating neurons from one another

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6
Q

oligodendrocytes

A

glial cells
produce myelin in CNS

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7
Q

Schwann cells

A

glial cells
produce myelin in the PNS

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8
Q

radial glia

A

guide migrating neurons and direct axonal outgrowth during development

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9
Q

astrocytes

A

glial cells
form the blood brain barrier

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10
Q

afferent neurons

A

carry information from periphery to the spinal cord via dorsal roots

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11
Q

efferent neurons

A

carry information from the spinal cord to the periphery via ventral roots

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12
Q

interneurons

A

carry information between neurons

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13
Q

spinal cord

A

contains white matter and grey matter
both dorsal horn (sensory) and ventral horn (motor)

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14
Q

white matter

A

nerve fibres, glia
lots of axons - myelinated

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15
Q

grey matter

A

neurons, glia, synapses
cell bodies - no myelin

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16
Q

neuron structure

A

dendrites
cell body (nucleus)
axon hillock
axon
synaptic terminals

flow of information = down axon, away from cell body

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17
Q

dendrites

A

receive stimuli through activation of chemically or mechanically gated ion channels

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18
Q

cell body

A

receives stimuli and produces excitatory and inhibitory postsynaptic potentials through activation of chemically or mechanically gated ion channels

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19
Q

axon hillock

A

trigger zone; integrates EPSPs and IPSPs → if sum causes depolarization that reaches threshold = initiation of action potential

site of action potential generation

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20
Q

axon

A

propagates nerve impulses from initial segment to axon terminals in a self-reinforcing manner
impulse amplitude does not change as it propagates along the axon

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21
Q

axon terminals

A

inflow of Ca2+ caused by depolarizing phase of nerve impulse triggers neurotransmitter release by exocytosis of synaptic vesicles

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22
Q

types of neurons

A

anatomy of neuron is dictated by function
bipolar cell
pseudo-unipolar cell
multipolar cell

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23
Q

bipolar cells

A

ex. retina
info from photoreceptors sent to retinal ganglion cells

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24
Q

pseudo-unipolar cells

A

afferent neurons
ex. ganglion cell of dorsal root

no real dendrites; peripheral axon conducts input from skin and muscle to the cell body
central axon exists between cell body and axon terminals

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25
Q

multipolar cells

A
  • motor - efferent - neuron of spinal cord (most typical representation of neuron)
  • pyramidal cell of hippocampus
  • purkinje cell of cerebellum
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26
Q

neuron structure

A

some neurons contain myelin sheath coating the axon = action potential is conducted faster
nodes of Ranvier are gaps in between myelin

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27
Q

membrane structure

A

phospholipid bilayer - impermeable barrier to ions

protein pumps and channels - control movement of ions through membrane

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28
Q

protein pumps

A

use energy by ATP hydrolysis for active transport

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29
Q

ion channels

A

are specific to ion
act as a door
do not require energy; move ions down electrochemical gradient

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30
Q

passive channels

A

leak channels
are open at rest

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31
Q

ligand-gated channels

A

closed at rest
ligand binds to receptor to open channel

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32
Q

voltage-gated channels

A

closed at rest
voltage change of neuron causes channel to open

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33
Q

resting membrane potential

A

steady state condition determined by relative permeability of membrane to to Na+ and K+
measure of electrical potential difference between intracellular environment and extracellular environment
resting membrane is approximately -70mV = inside the cell is ~70mV more negative than outside

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34
Q

Na+/K+ pump

A

sets net negative charge
electrogenic = moves charge across the membrane
requires energy (obtained from hydrolysis of ATP)
3Na+ molecules move out of cell and 2K+ molecules move in

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35
Q

mechanism of Na+/K+ pump

A

hydrolysis of ATP → P binds to pump on intracellular side = conformational change (close intracellular side of pump, open extracellular side)
3Na+ molecules are released outside of cell
2K+ molecules bind to inside of pump
phosphate is removed from binding site = conformational change (pump opens to inside of cell, closes to outside) → K+ moves into cell

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36
Q

Na+/K+ pump creates gradients

A

chemical: molecules want to maintain state of equilibrium
= K+ wants to diffuse out of cell; Na+ wants to diffuse into cell

electrical: intracellular environment wants to become more positive

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37
Q

leak channels

A

sets resting membrane
allow passive flow of ions into/out of neuron
selective for each ions

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38
Q

equilibrium potential

A

the membrane potential at which the chemical gradient is balanced

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39
Q

eq potential for K+

A

approximately -90mV

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40
Q

eq potential for Na+

A

approximately +60mV

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41
Q

membrane potential rule

A

the more permeant the ion, the greater its ability to force resting membrane potential towards its own equilibrium potential
more K+ leak channels than Na+

permeability is 50-100x greater to K+ than Na+

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42
Q

specific membrane resting potential

A

determined by specific proportion of Na+ and K+ leak channels

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43
Q

at resting membrane potential

A

passive ionic fluxes are balanced so that there is charge separation and Em remains constant

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44
Q

disruption of membrane potential

A

specific stimuli disrupt this steady state by causing ion-selective channels in membrane to open

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44
Q

action potential

A

large change in membrane potential from -70mV to +30mV and back to resting over a period of a few ms

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45
Q

generation of action potential

A

electrical signal is generated due to activity of voltage-gated Na+ and K+ channels
opening of channels = ions flow + membrane potential changes

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46
Q

activation of afferents

A

muscle stretch or other sensory stimuli → increased opening of specialized Na+ receptors
= entry of Na+ into afferent fibre and depolarization of afferent neuron

if Na+ entry is sufficient to depolarize the neuron to its threshold, the Na+ channels will open = action potentiak

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47
Q

activation gate

A

removed by depolarization
= allow Na+ to flow into cell

influx of Na+ into cells → brings membrane potential closer to Na+ equilibrium potential

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48
Q

inactivation gate

A

closes channel a few ms after opened

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49
Q

action potentials - summary

A
  1. rest
  2. depolarizing input
  3. start of action potential - depolarization
  4. repolarization phase
  5. end of action potential
  6. rest
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50
Q
  1. rest
A

relative permeability: K+&raquo_space; Na+

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51
Q
  1. depolarizing input
A

sensory or synaptic stimulus changes potential
relative permeability: increases to Na+

52
Q
  1. start of action potential - depolarization
A

Voltage-gated Na+ channels open
relative permeability: Na+&raquo_space;» K+

53
Q
  1. repolarization phase
A

voltage gated K+ channels open and Na+ channels inactivate
relative permeability: K+&raquo_space;» Na+

54
Q
  1. end of action potential
A

voltage gated Na+ channels at rest; voltage gated K+ channels still open
relative permeability: K+&raquo_space;» Na+

55
Q
  1. rest
A

voltage gated K+ channels at rest
relative permeability: K+&raquo_space; Na+

56
Q

action potentials: transmission

A

activation results in opening of voltage-gated Na+ channels = local depolarization of membrane
→ causes adjacent voltage-gated Na+ channels to activate
new action potential is generated in adjacent membrane
action potential only travels in one direction due to refractory period

57
Q

electrotonic conduction

A

spread of current inside axon

action potential initiated at one point in membrane
current spreads electrotonically to adjacent membrane
adjacent membrane depolarizes to threshold
new action potential generated in adjacent membrane

58
Q

speed of electrotonic conduction

A

current flow is fast but action potential must be regenerated at every point on the membrane = requires opening + closing of channels
slower than necessary for body functions

59
Q

myelination

A

increases speed of action potential propagation

only axon is myelinated

60
Q

myelin

A

fatty substance; acts as insulator → current can’t escape through channels in membrane
formed from Schwann cells in PNS; oligodendrocytes in CNS

61
Q

Nodes of Ranvier

A

small unmyelinated regions along axon
(myelination is discontinuous)

voltage-gated Na+ channels are clustered at nodes = where the action potential will need to be regenerated

62
Q

Schwann cell ensheathing

A

single Schwann cell generates single myelinated segment
= many Schwann cells required to ensheath one axon in the peripheral nervous system

63
Q

oligodendrocyte ensheathing

A

one oligodendrocyte ensheaths many axons in the CNS
a single oligodendrocyte lays down multiple segments of myelin on each fibre, on multiple fibres

64
Q

saltatory conduction

A

action potential is regenerated at nodes of Ranvier
current flows electrotonically between the nodes

65
Q

afferent fibre types

A

classification based on how fast they propagate action potentials:
- thickness of nerve fibre (axon)
- is it myelinated

66
Q

group I afferent fibres

A

diameter: 12-20 microns
conduction speed: 20-120 m/s
sensory receptors: skeletal muscle proprioceptor (ex. stretch reflex)

67
Q

group II afferent fibres

A

diameter: 6-12 microns
conduction speed: 35-75 m/s
sensory receptors: skin mechanoreceptor (touch/pressure afferents)

68
Q

group III afferent fibres

A

diameter: 1-5 microns
conduction speed: 5-30 m/s
sensory receptors: pain/temperature (quick + sharp pain)

69
Q

group IV afferent fibres

A

diameter: 0.2-1.5 microns
conduction speed: 0.5-2 m/s
sensory receptors: pain/itch/temperature (dull + throbbing pain)

70
Q

why does action potential conduct in only one direction?

A

by the time the absolute refractory period is over, the action potential is between 2 and 20 cm down the axon

action potential conduction:
- myelinated axons = 12-130 m/s
- unmyelinated axons = 0.5-2 m/s
absolute refractory period lasts almost 2 ms

71
Q

action potential transmission

A

sensory neuron fires action potential in response to physical stimulus → receptor potential → nerve ending is depolarized to threshold → action potential is generated in sensory neuron

72
Q

electrical synaptic transmission

A

physical channel connects two cells; physical coupling
no neurotransmitters; movement of molecules between cells
synchronize large groups of neurons to fire, especially during development

fast
bidirectional - no clear pre or post synaptic cell

73
Q

electrical synapses

A

gap junctions: small gap between the two cells is bridged by connexons → open or close to control the free flow of ions
communication between cytoplasm for sharing regulatory signals

inflexible - stereotypical behaviours, difficult to change response

74
Q

chemical synaptic transmission

A

release and binding of neurotransmitters between cells

75
Q

chemical synapses

A

much larger gap than electrical synapses
2 types:
- directly gated
- indirectly gated

flexible
inhibition, specificity, complexity, plasticity

76
Q

directly gated chemical synapse

A
  1. transmitter binds
  2. receptor channel located directly on ion channel opens
  3. ions pass through channel

receptor and effector are same molecule
effects: fast onset, short lasting

77
Q

excitatory transmission

A

glutamate: excitatory neurotransmitter
Na+ (+ K+) channels open → ions enter cell

78
Q

inhibitory transmission

A

GABA + glycine: inhibitory neurotransmitters
Cl- or K+ pass through = hyperpolarization of cell → no action potential

79
Q

indirectly gated chemical synapse

A
  1. transmitter binds
  2. activation of second messenger system
    GPCR → G proteins → adenylyl cyclase → cAMP = second messenger
  3. cAMP activates protein kinases
    → phosphorylation of ion channel → opens/closes + change in membrane permeability
  4. ion influx → depolarization or hyperpolarization

effects: slow onset, long lasting
receptor and effector are different molecules

80
Q

ionotropic receptor

A

in directly gated synapses
receptor is located on ion channel

81
Q

metabotropic receptor

A

in indirectly gated synapses
receptor is not directly located on effector; binding of transmitter induces intracellular cascade of events

82
Q

chemical synapse specificity

A

specific transmitters have specific effects on postsynaptic membrane

83
Q

chemical synapse complexity

A

response can vary in type, timecourse, strength, location, etc

84
Q

chemical synapse plasticity

A

changes in synaptic structure and function associated with development, aging, learning, etc.
indirectly gated synaptic transmission

85
Q

synaptic transmission

A
  1. action potential arrives in presynaptic terminal
  2. presynaptic terminal depolarizes
  3. voltage-gated Ca2+ hannels open
  4. Ca2+ influx into presynaptic terminal
  5. Ca2+ causes synaptic vesicles to fuse with presynaptic membrane
  6. transmitter released by exocytosis → diffuses across synapse → binds to receptor + opens ligand-gated ion channels
  7. ions flow across membrane as dictated by their concentration gradients and depolarize or hyperpolarize postynaptic cell
  8. transmitter removed from receptor → recycled or degraded
    ion channel closes and PSP ends
86
Q

excitatory presynaptic neuron

A

release of glutamate from presynaptic cell → binds to glutamate receptor on Na+ ion channel
channel opens → influx of Na+ = EPSP

87
Q

EPSP

A

excitatory postsynaptic potential
small depolarization resulting from influx of Na+
subthreshold (requires many to reach depolarization threshold)

88
Q

inhibitory presynaptic neuron

A

release of GABA or glycine from presynaptic cell → binds to Glu/gly receptor on Cl- ion channel
channel opens → influx of Cl- = IPSP

89
Q

IPSP

A

inhibitory postsynaptic potential
small hyperpolarization resulting from influx of Cl-
prevents generation of action potential

90
Q

synaptic potentials decay with distance

A

the potential of a depolarization loses amplitude as it travels down the dendrite - current leaks out membrane
the farther from the axon hillock the PSP’s site of origin is, the smaller it will be once it reaches the axon

91
Q

summation of PSPs

A

individually, a PSP is insufficient to generate an action potential
small PSPs can summate to reach threshold at axon hillock and trigger action potential

temporal and spatial summations occur simultaneously in the CNS

92
Q

temporal summation

A

PSPs from single presynaptic axon overlap in time → add together

93
Q

spatial summation

A

PSPs generated in different regions of the postsynaptic neuron are added together
the PSPs must also overlap in time

94
Q

spatial summation of EPSP and IPSP

A

IPSP cancels out the EPSP = very small potential

95
Q

synaptic integration

A

excitatory and inhibitory signals are integrated into a single response by the postsynaptic neuron
process of summing together all the inputs into an action potential output in the postsynaptic cell

96
Q

PSPs vs APs

A

PSP:
graded ~1mV
msec-sec
dendrites and soma of postsynaptic cell
passive

AP:
all-or-none
msec
initiated at axon hillock
active

97
Q

smooth muscle

A

walls of hollow organs
contraction reduces size of structures
not under voluntary control

98
Q

cardiac muscle

A

striated muscle
walls of the heart
no under voluntary control

99
Q

skeletal muscle

A

striated muscle
contraction is under voluntary control

100
Q

motor neuron

A

stimulates skeletal muscle cells to contract
1 efferent contacts lots of muscle cells

101
Q

motor unit

A

motorneuron + muscle fibres it activates
functional unit of motor system
smallest increment of force that can be generated

102
Q

synaptic transmission at neuromuscular junction

A

1 action potential in motor neuron = generation of 1 action potential in muscle cell (no PSPs)

each muscle fiber is only innervated by one presynaptic axon

always release of excitatory NT = Acetylcholine

axons are not myelinated = electrotonic conduction

103
Q

excitation contraction coupling

A

electrical signal of action potential is converted to mechanical force

104
Q

neuromuscular junction at rest

A

polarized = resting membrane potential
negative in cell; positive outside of cell

105
Q

release of acetylcholine

A

contained in vesicles
released into synaptic cleft by exocytosis

Ca2+ ions are pumped out of axon terminal

106
Q

contraction of muscle cell

A
  1. muscle action potential propagated down tranverse tubule → activates DHP receptor (bound to ryanodine receptor) = opening of Ca2+ channel
  2. Ca2+ released from sarcoplasmic reticulum into cytosol of cell
107
Q

DHP receptor

A

dihydropyridine receptor
voltage gated channel

108
Q

muscle fiber

A

myofibrils contain muscle filaments
sarcolemma: muscle fiber membrane
sarcoplasmic reticulum wraps around myofibrils; transverse tubules are in between SR

109
Q

sarcomere

A

segment of myofibril, in between two z disks
contains thick and thin filaments (alternate)

shortens during muscle contraction

110
Q

H zone

A

space between thin filaments
muscle contraction = shortening of H zone

111
Q

myosin

A

bundled together to form thick filaments
single molecule = tail + two globular heads (cross bridge)

112
Q

myosin cross bridge

A

two binding sites: ATP and actin

low energy state = bent, ATP is bound
high energy state = flat, ATP is hydrolyzed into ADP + P

113
Q

actin

A

primary component of thin filament
actin subunits are twisted into double helical chain
each subunit has myosin binding site

114
Q

tropomyosin

A

regulatory protein
entwines actin
at rest: tropomyosin covers myosin binding sites on actin subunits = cross bridge cannot bind

115
Q

troponin

A

attaches to tropomyosin strand
moves tropomyosin aside to expose myosin binding sites

has binding site for Ca2+

116
Q

sliding filament theory of muscle contraction

A
  1. influx of calcium triggers exposure of binding sites on actin
  2. myosin binds to actin
  3. power stroke of cross bridge
  4. ATP binds to cross bridge → disconnects from actin
  5. hydrolysis of ATP
  6. transport of Ca2+ into SR
117
Q
  1. exposure of binding sites on actin
A

Ca2+ ions flood into cytosol after release from SR → bind to troponin = change in conformation of troponin-tropomyosin complex
→ exposes binding sites on actin

118
Q
  1. binding of myosin to actin
A

high energy state myosin = cross bridge can bind to exposed actin site

119
Q
  1. power stroke
A

ADP + P are released from cross bridge (myosin is in low energy state)
cross bridge flexes → pulls thin filament inward toward center of sarcomere
H-zone shortens

= chemical energy → mechanical energy

120
Q
  1. disconnection of cross bridge from actin
A

ATP molecule must bind to site on myosin cross bridge to release myosin from thin filament

121
Q
  1. hydrolysis of ATP
A

ATP is hydrolyzed → ADP + P
re-energizing + repositioning of cross bridge
myosin = high energy state

122
Q
  1. removal of Ca2+ ions
A

active transport from cytosol into SR by calcium pumps (membrane of SR) → energized by ATP

calcium is removed → troponin-tropomyosin complex covers binding sites on actin

123
Q

multiple cross bridge cycles

A

during a contraction, all cross bridges are neither bound nor disconnected at the same time

124
Q

role of ATP in muscle contraction

A
  1. energizing power stroke
  2. disconnecting cross bridge from actin
  3. pumping Ca2+ back into SR
125
Q

white muscle fiber

A

large
light in colour → reduced myoglobin
few capillaries
few mitochondria
high glycogen content

glycolysis: anaerobic process to generate large amounts of ATP fast
quickly depleted

126
Q

red muscle fiber

A

half the diameter of white fibers
dark red → lots of myoglobin
many capillaries
lots of mitochondria
low glycogen content

oxidative phosphorylation + Krebs cycle: aerobic processes to generate ATP (slower process)
slower deletion of ATP

127
Q

fast twitch fibers

A

white muscle fibers
power and speed; short duration
glycolysis = quick synthesis of ATP
fast contractions
large number of myofilaments
fatigue rapidly - build up of lactic acid, depletion of glycogen

128
Q

slow twitch fibers

A

red muscle fibers
endurance, continuous contraction
Krebs cycle + oxidative phosphorylation
slower contractions