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*NEUROMUSCULAR ASPECTS OF EXERCISE > SLE1/MODULE 3- Synaptic Transmission > Flashcards

SLE1/MODULE 3- Synaptic Transmission Flashcards

1
Q

what is sodium’s equilibrium potential

A

typically around +55 mV

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2
Q

synapse

A

before AP initiates + propagates, a cell receives current inputs to change the membrane potential (Vm)

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3
Q

what occurs at a synapse

A

a specialized connection enabling a change in membrane potential (Vm) in one cell to be transmitted to another
-presynaptic cell -> postsynaptic cell

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4
Q

2 types of neurons

A

-presynaptic
-postsynaptic

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5
Q

2 types of synapses

A

-electrical
-chemical

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6
Q

electrical synapse

A

direct transmission of current between 2 cells (presynaptic + postsynaptic)

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7
Q

chemical synapse

A

release of chemical agent by presynaptic cell to attach to postsynaptic cell, eliciting a change in membrane potential (Vm)

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8
Q

myelin

A

allows for movement of current for charges to be FASTER

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9
Q

what creates myelin

A

glial cells

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10
Q

what glial cells create myelin in CNS

A

oligodendrocytes

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11
Q

what glial cells create myelin in PNS

A

Schwann cells

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12
Q

what does speed of AP propagation depend on

A

whether or not there is myelin
-whether or not there is more myelin
-fewer nodes
-etc.

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13
Q

an AP will propagate quicker if there is myelin or nodes

A

myelin

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14
Q

when there is myelin, what happens

A

appears that AP is jumping from one node to another
-saltatory conduction

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15
Q

how do nodes make AP faster

A

there is a greater density of voltage gated sodium channels, allowing for greater depolarization
-more channels/conductors = ions can move through doorways quicker + have more effective impact

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16
Q

where are APs generated

A

axon hillock

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17
Q

describe AP generation

A

APs are generated at the axon hillock when there is enough depolarization ->
AP will propagate downwards towards node 1 ->
if there is enough sodium that influxes to depolarize, the AP will propagate to node 2 ->
same thing to node 3

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18
Q

why are APs generated at the axon hillock

A

it is the first place that membrane potentials accumulate
-this is where it is determined if an AP is going to occur or not

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19
Q

what makes the axon hiloock special

A

HAS HIGHEST DENSITY OF SODIUM CHANNELS

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20
Q

where are the most sodium channels found

A

axon hillock

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21
Q

gap junction

A

little separators between the presynaptic + postsynaptic neuron

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22
Q

another name for gap junctions

A

electrical synapses

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23
Q

what do gap junctions (electrical synapses) allow for

A

-high conductance/passage
-high capacity for electrical current to flow in either direction

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24
Q

describe gap junction role in AP generation

A

-voltage gated ion channels in presynaptic cell will generate electrical current, which will pass through the gap junction; WE MUST DO THIS FOR AN AP TO START
-if there are enough gap junctions, you will be able to get more current through from the presynaptic to postsynaptic neuron + you will get AP generation

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25
Q

what do gap junctions do

A

MOVE CURRENT/ MOVE CHARGES

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26
Q

why are gap junctions referred to as electrical synapses?

A

because they are conducting electricity

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27
Q

what do gap junctions conduct

A

charges, charged ions

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28
Q

cell-to-cell adhesions are also called

A

membrane junctions

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29
Q

cell-to-cell adhesions (membrane junctions)

A

use plasma membrane to put things near each other (only those cells that want to be tightly packed)

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30
Q

3 types of cell-to-cell adhesions (membrane junctions)

A

-tight junctions
-desmosomes
-gap junctions

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31
Q

tight junctions

A

serve to seal adjacent cells together so that fluids cannot leak between them (fluid barrier)

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32
Q

desmosomes

A

anchor adjacent cells together to resist pulling forces (anchoring junctions)

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33
Q

gap junctions

A

provide a “tunnel” between adjacent cells allowing direct electrical + metabolic coupling of the cells

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34
Q

metabolic coupling

A

capillaries, tiny blood vessels that don’t contact all the cells of the body so all the cells can’t get nutrients in discrete ways SO you need gap junctions for tissue like skin like avascular tissue to get rid of waste + get nutrients in

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35
Q

where are gap junctions found

A

many places throughout the body

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36
Q

intercellular communciation

A

cell-to-cell interaction is necessary for homeostasis

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37
Q

direct intercellular communication

A

gap junctions

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38
Q

indirect intercellular communication

A

chemical messengers used
-chemical messenger is released by 1 cell
-receptors on different (target) cell

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39
Q

indirect/direct communication always take more time/effort

A

indirect
-think about communicating with a friend through another person; takes more time/effort
-direct method is much faster

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40
Q

gap junctions

A

comprise pair of channels in the membranes of the presynaptic + postsynaptic cells
-direct electrical coupling between 2 cells

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41
Q

are gap junctions small/large

A

large enough to permit passage of ions contribution to membrane potential

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42
Q

gap junctions are fast/slow

A

very rapid

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43
Q

gap junctions are passive/active

A

passive
-signal can degenerate
-if I travel from node 1 to node 3, there is a possibility that the signal is no longer strong enough + the AP dissipates

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44
Q

gap junctions are unidirectional/bidirectional

A

bidirectional
-can go one way or another
-CANNOT go backwards until refractory period ends

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45
Q

gap junctions are depolarizing/hyperpolarizing

A

either

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46
Q

neurotransmitters are slow/fast

A

relatively slow
-0.5 ms

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47
Q

neurotransmitters are the primary synapse in what

A

human movement

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48
Q

what do neurotransmitters attach to

A

ligand or voltage gated receptors/channels

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49
Q

where are neurotransmitters storeed

A

in synaptic vesicles

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50
Q

where are neurotransmitters removed

A

in the synaptic cleft

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51
Q

2 types of neurotransmitters

A

-small-molecule transmitters
-neuroactive peptides (short polymers of amino acids)

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52
Q

what are neurotransmitters influenced by

A

-concentration
-types of ions along membrane

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53
Q

what do ions flow through

A

postsynaptic channels

54
Q

what is determined by binding at the postsynaptic cell

A

whether the impact is excitatory/inhibitory

55
Q

how far apart are presynaptic + postsynaptic neuron membranes

A

20-40 nm

56
Q

AP steps

A

AP from presynaptic cell travels to end bulb ->
calcium enters ->
due to the influx of calcium, vesicles fuse to the presynaptic membrane + exit into the presynaptic cleft ->
vesicles release neurotransmitters into synaptic cleft ->
neurotransmitters attach to specific receptors + open them to allow ions to move to the postsynaptic neuron ->
the influx of ions changes the postsynaptic neuron membrane potential + generates an AP

57
Q

more summarized AP steps

A

AP in presynaptic cell ->
release of neurotransmitters stored in vesicles of presynaptic terminals ->
ligand-gated channels receive neurotransmitter in postsynaptic cell, opening ion channels ->
change in cell memrbane potential postsynaptically

58
Q

what do specialized channels allow for

A

influx of calcium when needed
-needed to communicate/move charged particles

59
Q

how can we identify a neuromuscular junction

A

-there will be many labels for ACh
-motor end plate

60
Q

ACh

A

neurotransmitter at the neuromuscular junction at the last synapse before we get to muscle contraction

61
Q

motor end plate

A

postsynaptic terminal at the neuromuscular junction

62
Q

what releases ACh

A

terminal button (the swellings formed by several branches at the axon)

63
Q

ACh impact

A

significant impact on changes in the membrane potential at the muscle + results in muscle contraction/reduction in muscle contraction

64
Q

what is found in the folds of the membrane

A

high density of ACh receptors
-ACh will be released but degrade VERY QUICKLY

65
Q

why does degradation of ACh occur after release

A

due to enzymatic hydrolysis by acetylcholinesterase

66
Q

acetylcholinesterase

A

an enzyme that causes rapid hydrolysis of ACh
-responsible for stopping the excitation of the nerve after the transmission of an AP
-diffuses across end plate receptors

67
Q

**what is the neurotransmitter that is key to creating an AP at the neuromuscular junction

A

ACh

68
Q

motor neuron

A

the neuron that connects the spinal cord to the neuromuscular system

69
Q

steps in neuromuscular transmission/propagation

A

arrival of AP in motor neuron ->
opening of voltage gated Ca2+ channels, causing influx of Ca2+ ->
exocytosis of ACh, transfer + fusion vesicles containing ACh to presynaptic terminal ->
release of ACh in synaptic cleft + binding to receptors on ion channels ->
ion channels open ->
influx of Na+ and efflux of K+ causing depolarization of the membrane potential ->
generate AP

70
Q

when does neuromuscular transmission stop

A

when ACh is removed from synaptic cleft

71
Q

2 ways that ACh is removed from synaptic cleft

A

-ACh diffuses away from synapse
-ACh is broken down by enzyme acetylcholinesterase into acetic acid + choline

72
Q

3 types of impairments

A

-receptor blockers
-degradation prevention
-diseases of neuromuscular junction

73
Q

impairments- receptor blockers

A

receptor antagonist blocks ACh receptor

74
Q

impairments- degradation prevention

A

-anticholinesterase drugs prevent the breakdown of ACh
-used to paralyze muscle during surgical procedures

75
Q

impairments- diseases of the neuromuscular junction

A

-genetic transmission
-poor ACh packaging
-receptor impairments
-ACh enzyme mismanagement

76
Q

Lambert-eaten myosthenic syndrome

A

immune disorder that influences neuromuscular junction
-destroys voltage gated calcium channels

77
Q

myasthenias

A

involve weakness of musculature
-weakness varies day to day, as well as throughout the day
-there are experimental set ups you can implement to determine whether someone has 1 myasthenia syndrome vs another

78
Q

which prominent syndrome results from myasthenia gravis, a disorder in which ACh receptors are targeted by the immune system, resulting in fewer ACh receptors

A

you will still be able to produce force, BUT LESS
-primary weakness of musculature occurs

79
Q

where is first affected in myasthenia gravis

A

ocular/eye muscle weakness first
-then moves to muscles that affect swallowing, talking, chewing, etc.

80
Q

how can myosthenia gravis be detected

A

through antibiodies through ACh receptors in the plasma

81
Q

botox

A

bacterium clostridium botulinum
-potent neurotoxin that disrupts transmission as a chemical synapse

82
Q

how does botox work

A

one part of the protein disables fusion proteins at the NMJ

83
Q

how is botox administered

A

by injection into a muscle where it is transported by endocytosis into presynaptic terminals

84
Q

paralysis via botox depends on what

A

dose

85
Q

when does botox paralysis peak

A

at 5-8 days after the injection

86
Q

how long does botox paralysis last

A

3 months

87
Q

effects of botox

A

the disable of fusion proteins is permanent + causes some atrophy + demyelination of the axon

88
Q

after botox, what does initial recovery of muscle function require

A

requires axon to develop sprouts + establish new synaptic contacts

89
Q

what can repeated botox injections cause

A

can cause NMJs to become abnormal

90
Q

can botox be transported retrogradely

A

yes- can be transported retrogradely back to the motor neuron + disrupts the function of central synapses

91
Q

protocol for botox for wrinkles

A

injections into muscles every 3-6 months

92
Q

medical uses for botox

A

-migraines
-back pain
-stuttering
-carpal tunnel syndrome
-overactive bladder
-multiple sclerosis
-cerebral palsy (spasticity)
-excessive sweating
-cervical dystonia

93
Q

botox- what doesn’t work + what happens as a result

A

fusion proteins (proteins allowing vesicles with ACh to exocytose) do not work, so no ACh is release
-this is ultimately the thing that causes the muscle cell to not contract/have a reduction in contraction

94
Q

if there is not an adequate amount of botox what would happen

A

reduction in muscle contraction

95
Q

EPSP

A

excitatory post synaptic potentials

96
Q

IPSP

A

inhibitory post synaptic potentials

97
Q

synaptic integration

A

neurons receive currents that produce responses that can be excitatory/inhibitory postsynaptic potentials (EPSP or IPSP)

98
Q

what does the amplitude of net excitatory PSP depend on

A

the sum of inputs (summation)
-if i have a bunch of excitatory coming in but also a bunch of inhibitory, I will have a net that is less than the big excitatory signal

99
Q

2 types of summation

A

-spatial
-temporal

100
Q

spatial summation

A

signal comes from multiple synapses or locations

101
Q

types of spatial synapses

A

-axodendritic synapse
-axosomatic synapse
-axoaxonic synapse

102
Q

axodendritic synapse

A

axon of presynaptic neuron connects to dendrite of postsynaptic neuron

103
Q

axosomatic synapse

A

axon of presynaptic neuron latches to cell body/soma of postsynaptic neuron

104
Q

axoaxonic synapse

A

axon of presynaptic neuron connects to axon of postsynaptic neuron

105
Q

*see slides 30 + 31 image of types of spatial synapses

A
106
Q

temporal summation

A

synapses come in a QUICK SUCCESSION from the SAME neuron

107
Q

where does a neuron receive inputs

A

at the dendrites

108
Q

where is AP generated

A

at axon hillock

109
Q

where is AP transmitted along

A

along the axon to the target cells

110
Q

where do most synapses that deliver info to the neuron occur

A

at the dendrites
-many of them on dendritic spines (the little knobs coming off of the dendrites)

111
Q

dendrites

A

branches coming out of the soma/cell body

112
Q

neuromodulation

A

the signals we get can be modulated
-summation is a way of modulating signals

113
Q

what do neuromodulatory receptors do

A

increase responses that are evoked/caused by synaptic transmission
-these changes affect the ion channels + even change the things that happen afterwards with the postsynaptic receptor

114
Q

2 types of neuromodulation

A

-presynaptic inhibition
-presynaptic facilitation

115
Q

imagine there is a postsynaptic membrane with a bunch of receptors. if ions bind to modify/neuromodulate, what happens afterwards…

A

everything that happens afterwards is through SECOND MESSENGERS
-a bunch of things can affect how much or if at all the second messengers at the end of the postsynaptic terminal actually make things happen

116
Q

presynaptic inhibition

A

occurs as an axon makes synaptic contact with another axon
-reduces amount of transmitter (CALCIUM) released by a presynaptic cell in response to an AP

117
Q

what is a blip that doesn’t hit threshold called

A

EPSP

118
Q

presynaptic facilitation

A

augment the influx of calcium into the presynaptic terminal + prolong the postsynaptic potential
-augment the influx of calcium into the presynaptic terminal + prolong the postsynaptic potential

119
Q

what color do we typically color INHIBITORY neurons

A

black

120
Q

what color for excitatory

A

beige

121
Q

movement along an axon can be ____

A

bidirectional

122
Q

axonal transport system

A

there are proteins (microtubules + other fibular elements) that regulate the stability + orientation of the cytoskeleton of the neuron

123
Q

axonal transport along the cytoskeleton occurs in what directions

A

bidirectional
-both directions, forwards + backwards (anterograde/orthograde or retrograde)

124
Q

anterograde/orthograde

A

movement of signals away from the soma

125
Q

anterograde/orthograde axonal transport is driven by which enzyme

A

kinesin enzyme

126
Q

retrograde

A

movement of the signals back toward the soma

127
Q

retrograde axonal transport is driven by which enzyme

A

cytoplasmic dynein enzyme (molecular motor)

128
Q

if a signal is coming in externally (Artificial stimualtion), you can have signals going in which directions

A

both ways from the location of the input
-BIDIRECTIONAL

129
Q

if the signal is coming internally (ex: AP created because sent a voluntary signal from brain downstream)…what will occur

A

there will be a refractory period
-CANNOT HAVE A SIGNAL RETROGRADE AS WE ARE GOING ANTEROGRADE/ORTHOGRADE

130
Q

what can axonal transport impact

A

the properties of nerve + muscle cell
(neurogenic or myogenic)

131
Q

neurogenic

A

axonal transport from nerve to muscle
-ex: a nerve is cut
-impacts nervous system + muscular system, requires neurogenic factors to regulate normal properties of nerve-muscle system

132
Q

myogenic

A

axonal transport from muscle to nerve

*NEUROMUSCULAR ASPECTS OF EXERCISE (9 decks)

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