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Physiology > Lecture 5 > Flashcards

Lecture 5 Flashcards

1
Q

This type of synapse is separated by a Gap-junction channel:

A

electrical synapse

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2
Q

This type of synapse is separated by a synaptic cleft:

A

chemical synapse

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3
Q

Majority of synapses in the CNS and PNS are mediated by:

A

chemical synapse

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4
Q

This type of synapse involves a presynaptic cell whereas this type involves a presynaptic cleft:

A

electrical, chemical

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5
Q

This type of synapse is formed by hemichannels:

A

electrical (also called connexons)

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6
Q

T or F? A synapse transmits intracellular signals.

A

F. Intercellular

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7
Q

Intercellular signals can be either:

A

electrical or chemical

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8
Q

These mediate electrical or electronic transmission:

A

gap junctions

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9
Q

Gap junctions are generally (excitatory/inhibitory)

A

excitatory

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10
Q

T or F? Chemical signals mediate only excitation.

A

F. either excitation or inhibition

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11
Q

What type of channel does an AP open in the nerve terminal of a presynaptic cell?

A

Ca

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12
Q

What causes vesicle fusion?

A

Ca entry

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13
Q

What causes transmitter release?

A

Ca entry

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14
Q

Wat type of channel does an AP open in the postsynaptic cell?

A

Na receptor-channels

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15
Q

This type of channel is both receptor and channel:

A

Na

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16
Q

How do currents from a presynaptic AP affect the postsynaptic PM?

A

they don’t, they are shunted in the synaptic cleft

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17
Q

T or F? transmitter-receptor binding can produce a depolarization or hyperpolarization of the PM.

A

T

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18
Q

This is a special synapse bw neuron and skeletal muscle:

A

NMJ

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19
Q

Where is the cell body of the neuron located?

A

Spinal cord

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20
Q

This is a ‘giant’ excitatory synapse:

A

NMJ

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21
Q

What ensures high transmission reliability at the NMJ?

A

large size of synapse

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22
Q

In the absence of disease, 1 nerve AP generates:

A

1 muscle AP

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23
Q

Another name for NMJ

A

endplate potential

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24
Q

Motor unit:

A

1 motor neuron + all fibers it innervates

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25
Q

T or F? Each muscle fiber can be innervated by multiple motor neurons.

A

F. Only one

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26
Q

Does an alpha neuron typically innervate one or more than one muscle fiber?

A

more than one

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27
Q

Is the motor neuron cell body in the dorsal or ventral horn?

A

ventral

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28
Q

A motor neuron is connect to a ____ via a NMJ:

A

myofiber

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29
Q

Are NMJ junctions bigger the in the CNS or PNS?

A

PNS (check, note just say “huge compared to CNS”)

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30
Q

Do small neuron or large neurons have a higher reliability of transmission?

A

large

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31
Q

What type of cell is the outer surface of the presynaptic terminal bouton made of?

A

Schwann cells, a sheath

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32
Q

NMJs innervate:

A

muscle fibers

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33
Q

This allows for the axon terminal to contact a large MF surface area:

A

terminal arborization

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34
Q

Axon terminal boutons lie in:

A

gutter-like invaginations with in-foldings of the MF surface

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35
Q

What forms primary and secondary synaptic clefts?

A

unfolded junctional surface

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36
Q

How much transmitter does each vesicle contain?

A

1 quantum

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37
Q

How many AcH molecules are in one quantum?

A

5,000-10,000 molecules

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38
Q

Vesicles are divided into these 2 pools:

A

small readily releasable and large stationary (slow releasable)

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39
Q

Are the sole releasable pool vesicles located nearer or farther from the PM?

A

farther

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40
Q

Another name for large stationary vesicles:

A

slow releasable

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41
Q

What anchors AChE?

A

ECM

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42
Q

These cleft are blank spaces while these contain AChE:

A

CNS, PNS

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43
Q

What is the transmitter release site called?

A

active zone

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44
Q

The majority of AChRs are this type of receptor, each made up of this many subunits:

A

Nicotinic receptors - 5 subunits (pentameric)

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45
Q

What type of channel is nAChR?

A

an ACh-gated non-selective cationic channel

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46
Q

List the subunit of the nAChR:

A

2 alpha, 1 beta, 1 gamma, 1 delta

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47
Q

Where is there a high density of AChRs?

A

in the crests of postsynaptic folds

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48
Q

T or F? Negative charged ions will flow through the cACHRs:

A

F. Positively charged will

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49
Q

this is a non-conductance state:

A

densitized R

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50
Q

How long of a delay is there with chemical transmission?

A

about 0.5 msec

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51
Q

What triggers exocytosis of vesicles docked at the active zones?

A

increase in Ca conc.

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52
Q

How many active zones are found in one NMJ?

A

200-300

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53
Q

What is an active zone?

A

a release site

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54
Q

How many quantum are released at the active zone per nerve AP?

A

1 quantum (200-300 quanta)

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55
Q

Another name for muscle AP:

A

muscle EPP

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56
Q

How can you mobilize more vesicles from the stationary pool?

A

increase nerve AP freq. (increase Ca conc)

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57
Q

Are nicotinic receptors both receptor and channel?

A

Yes

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58
Q

EPP are due to:

A

activation of AcH receptor

59
Q

T or F? The threshold for an EPP is always bigger (more negative) than the threshold for firing an AP of the muscle.

A

T.

60
Q

T or F? Frequency codes for amplitude.

A

F?

61
Q

What does frequency code for?

A

info

62
Q

Is the activation threshold larger at the presynaptic end or postsynaptic end?

A

post (-80 vs. -70)

63
Q

What type of channels are activated by a NAP?

A

voltage-gated Ca channels

64
Q

Does the K driving force get bigger or smaller with the influx of Na?

A

bigger

65
Q

Does the Na driving force get bigger or smaller with the influx of Na?

A

smaller

66
Q

T or F? Na/K channels are selective.

A

F. non-selective

67
Q

Neurons going to EPP are only (excitatory/ inhibitory)

A

excitatory

68
Q

In normal conditions, an EPP is always a _______ potential that produces an AP in the skeletal muscle.

A

supra-threshold

69
Q

Does an EPP have a large or small safety margin, and how big is it?

A

large, about 30mV

70
Q

At which point of the graph is the current of the EPP zero?

A

at the peak, the driving force of Na and K cancel each other out

71
Q

At what point on the graph do the AChRs deactivate?

A

at the reversal potential, peak of the graph

72
Q

T or F? EPP is presynaptic.

A

F. Post

73
Q

The amplitude of the EPP (decreases/increases) as it moves away from the EP region.

A

decreases

74
Q

The safety margin for generating a MAP is the voltage separation bw the:

A

threshold and the reversal potential

75
Q

How can you determine the EPP?

A

block more and more receptors until it will no the tablet o pass threshold

76
Q

EPP is an example of a ___ electronic (local) potential.

A

decrementing

77
Q

A large enough ___ must be created to pass threshold:

A

EPP

78
Q

How can you decrease a graded potential?

A

reduce activated receptors or block release of transmitter

79
Q

2 types of AcHR’s:

A

nicotinic and GPCR

80
Q

What does the graded potential depend upon?

A

the amount of ACh released and the number of nAChR activated

81
Q

T or F? The graded potential is an all-or-nothing potential.

A

F.

82
Q

T or F? The EPP will continue to increase in size at a high rate of stimulation.

A

F. Increase at first then decrease due to depletion of vesicles

83
Q

Why do the number of vesicles deplete at high frequency stimulation over time?

A

can’t recycle the vesicles fast enough

84
Q

A high rate of stimulation produces:

A

facilitation

85
Q

What causes an increase in the amount of quanta released?

A

increase in Ca conc

86
Q

About what fraction of ACh is hydrolyzed upon release?

A

1/3

87
Q

3 fates of ACh after release into the junctional cleft:

A
  1. diffusion out of cleft
  2. AChE (reuptake)
  3. AChR (at the post junctional fold)
88
Q

AcH breaks down to:

A

acetate and choline

89
Q

This is the only example in which transmitter action is terminated by enzymatic action:

A

ACh

90
Q

List reversible ACh inhibitors:

A

physostigmine (eserine) and neostigmine

91
Q

List irreversible ACh inhibitors:

A

organophosphorus (used in sarin gas & insecticides)

92
Q

How would an increase in ACh function affect Alzheimers pts?

A

it would help cognition

93
Q

What does termination of transmitter action depend upon?

A

diffusion out of cleft

94
Q

Can ACh participate in multiple bindings if the transmitter remains in the cleft?

A

yes

95
Q

How is the vesicle membrane retrieved after fusion with the PM?

A

endocytosis

96
Q

Vesicle endocytosis is ______ dependent.

A

Clathrin

97
Q

Vesicle membrane is linked to clathrin endocytic machinery via:

A

adaptor proteins

98
Q

What happens to vesicles that are not recycled?

A

They are depleted

99
Q

2 pathways recycled vesicle membrane can take:

A

direct or indirect (back to membrane or to ER)

100
Q

Nicotinic receptor is AKA:

A

ionotropic

101
Q

This type of cholinergic receptor directly activates an ion channel:

A

nicotinic ionotropic

102
Q

This type of cholinergic receptor indirectly affects conductance of many channels via intracellular signaling:

A

muscarinic metabotropic

103
Q

This type of cholinergic receptor is located in the NMJ:

A

nicotinic ionotropic

104
Q

All autonomic ganglia and some CNS synapses use this type of cholinergic receptor:

A

nicotinic ionotropic

105
Q

Are nicotinic receptors ionotropic or metabotropic?

A

ionotropic

106
Q

Are muscarinic receptors ionotropic or metabotropic?

A

metabotropic

107
Q

This type of receptor can only activate GpCoupled intracellular signaling:

A

muscarinic metabotropic

108
Q

how do muscarinic metabotropic receptors affect conductance of many channels?

A

via intracellular signalling

109
Q

This type of receptor is located at neuroeffector junctions:

A

muscarinic metabotropic (glands, s.m. tissues and some CNS synapses

110
Q

Agents that activate receptors:

A

agonists

111
Q

T or F? succinylcholine is hydrolyzed by AChE:

A

F.

112
Q

Prolonged exposure to an agonist leads to:

A

desensitization

113
Q

These can bind but can’t activate receptors:

A

antagonist

114
Q

Agonists and antagonists compete by:

A

mass action for binding the same receptor

115
Q

Toxins blocking neuromuscular transmission:

A

botulinum toxin and alpha-bungarotoxin

116
Q

botulinum toxin blocks:

A

exocytosis of vesicles

117
Q

alpha-bungarotoxin blocks:

A

activation by ACh

118
Q

How does botulinum toxin block exocytosis of vesicles?

A

proteolytically cleaving components of vesicle fusion machinery in presynaptic terminals

119
Q

How does alpha-bungarotoxin block activation by ACh?

A

a small basic peptide binds AChR irreversible

120
Q

This toxin block neuromuscular transmission bc there is no release of transmitter;

A

botulinum toxin

121
Q

botulinum toxin is produced by:

A

Clostridium botuminum

122
Q

alpha-bungarotoxin is produced by:

A

banded krait snake, Bungarus multicinctus

123
Q

Focal intoxication with botulinum toxin produces:

A

a chronic denervated state

124
Q

This toxin works postsynaptically:

A

alpha-bungarotoxin

125
Q

This toxin works presynaptically:

A

botulinum toxin

126
Q

This toxin is a receptor agonist:

A

alpha-bungarotoxin

127
Q

This is an autoimmune postsynaptic disease that impairs NM transmission:

A

myasthenia gravis

128
Q

Effect of myasthenia gravis:

A

muscle weakness

129
Q

2 diseases of the neuromuscular junction:

A

myasthemia gravis and Lambert-Eaton myasthenic syndrome

130
Q

Autoantibodies against AChRs cause:

A
  1. loss of AChRs and increased rate of turnover in junctional PM
  2. local inflammatory reaction and widening of synaptic clefts
131
Q

The effect of myasthenia gravis lead to the loss of the:

A

safety margin

132
Q

Why does myasthenia gravis lead to muscle weakness?

A

bc the loss of safety margin makes it harder to reach the threshold

133
Q

T or F? Autoantibodies increase the reliability of signal transmission.

A

F. decrease

134
Q

What do autoantibodies block?

A

postsynaptic receptors

135
Q

Do nicotinic receptor desensitizes quickly or slowly?

A

quickly

136
Q

This is autoimmune presynaptic disease that impairs NM transmission:

A

Lambert-Eaton myasthenic syndrome

137
Q

This NM disease is presynaptic while this is one postsynaptic:

A

Lambert-Eaton myasthenic syndrome, myasthenia gravis

138
Q

in this NM disease autoantibodies are against specific class of Ca2+ channel:

A

Lambert-Eaton myasthenic syndrome

139
Q

In Lambert-Eaton myasthenic syndrome autoantibodies are against:

A

specific class of Ca2+ channel

140
Q

The only 2 agents that are excitatory at the NMJ:

A

ACh and nicotine

141
Q

Effect of tetra toxin:

A

block nerve AP

142
Q

Affect of bungarotoxin:

A

impair transmission

143
Q

Affect of blocking AChE:

A

prolong the action of ACh

Physiology (55 decks)

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