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Flashcards in Lecture 5 Deck (143):
1

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

electrical synapse

2

This type of synapse is separated by a synaptic cleft:

chemical synapse

3

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

chemical synapse

4

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

electrical, chemical

5

This type of synapse is formed by hemichannels:

electrical (also called connexons)

6

T or F? A synapse transmits intracellular signals.

F. Intercellular

7

Intercellular signals can be either:

electrical or chemical

8

These mediate electrical or electronic transmission:

gap junctions

9

Gap junctions are generally (excitatory/inhibitory)

excitatory

10

T or F? Chemical signals mediate only excitation.

F. either excitation or inhibition

11

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

Ca

12

What causes vesicle fusion?

Ca entry

13

What causes transmitter release?

Ca entry

14

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

Na receptor-channels

15

This type of channel is both receptor and channel:

Na

16

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

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

17

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

T

18

This is a special synapse bw neuron and skeletal muscle:

NMJ

19

Where is the cell body of the neuron located?

Spinal cord

20

This is a 'giant' excitatory synapse:

NMJ

21

What ensures high transmission reliability at the NMJ?

large size of synapse

22

In the absence of disease, 1 nerve AP generates:

1 muscle AP

23

Another name for NMJ

endplate potential

24

Motor unit:

1 motor neuron + all fibers it innervates

25

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

F. Only one

26

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

more than one

27

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

ventral

28

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

myofiber

29

Are NMJ junctions bigger the in the CNS or PNS?

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

30

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

large

31

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

Schwann cells, a sheath

32

NMJs innervate:

muscle fibers

33

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

terminal arborization

34

Axon terminal boutons lie in:

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

35

What forms primary and secondary synaptic clefts?

unfolded junctional surface

36

How much transmitter does each vesicle contain?

1 quantum

37

How many AcH molecules are in one quantum?

5,000-10,000 molecules

38

Vesicles are divided into these 2 pools:

small readily releasable and large stationary (slow releasable)

39

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

farther

40

Another name for large stationary vesicles:

slow releasable

41

What anchors AChE?

ECM

42

These cleft are blank spaces while these contain AChE:

CNS, PNS

43

What is the transmitter release site called?

active zone

44

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

Nicotinic receptors - 5 subunits (pentameric)

45

What type of channel is nAChR?

an ACh-gated non-selective cationic channel

46

List the subunit of the nAChR:

2 alpha, 1 beta, 1 gamma, 1 delta

47

Where is there a high density of AChRs?

in the crests of postsynaptic folds

48

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

F. Positively charged will

49

this is a non-conductance state:

densitized R

50

How long of a delay is there with chemical transmission?

about 0.5 msec

51

What triggers exocytosis of vesicles docked at the active zones?

increase in Ca conc.

52

How many active zones are found in one NMJ?

200-300

53

What is an active zone?

a release site

54

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

1 quantum (200-300 quanta)

55

Another name for muscle AP:

muscle EPP

56

How can you mobilize more vesicles from the stationary pool?

increase nerve AP freq. (increase Ca conc)

57

Are nicotinic receptors both receptor and channel?

Yes

58

EPP are due to:

activation of AcH receptor

59

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

T.

60

T or F? Frequency codes for amplitude.

F?

61

What does frequency code for?

info

62

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

post (-80 vs. -70)

63

What type of channels are activated by a NAP?

voltage-gated Ca channels

64

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

bigger

65

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

smaller

66

T or F? Na/K channels are selective.

F. non-selective

67

Neurons going to EPP are only (excitatory/ inhibitory)

excitatory

68

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

supra-threshold

69

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

large, about 30mV

70

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

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

71

At what point on the graph do the AChRs deactivate?

at the reversal potential, peak of the graph

72

T or F? EPP is presynaptic.

F. Post

73

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

decreases

74

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

threshold and the reversal potential

75

How can you determine the EPP?

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

76

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

decrementing

77

A large enough ___ must be created to pass threshold:

EPP

78

How can you decrease a graded potential?

reduce activated receptors or block release of transmitter

79

2 types of AcHR's:

nicotinic and GPCR

80

What does the graded potential depend upon?

the amount of ACh released and the number of nAChR activated

81

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

F.

82

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

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

83

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

can't recycle the vesicles fast enough

84

A high rate of stimulation produces:

facilitation

85

What causes an increase in the amount of quanta released?

increase in Ca conc

86

About what fraction of ACh is hydrolyzed upon release?

1/3

87

3 fates of ACh after release into the junctional cleft:

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

88

AcH breaks down to:

acetate and choline

89

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

ACh

90

List reversible ACh inhibitors:

physostigmine (eserine) and neostigmine

91

List irreversible ACh inhibitors:

organophosphorus (used in sarin gas & insecticides)

92

How would an increase in ACh function affect Alzheimers pts?

it would help cognition

93

What does termination of transmitter action depend upon?

diffusion out of cleft

94

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

yes

95

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

endocytosis

96

Vesicle endocytosis is ______ dependent.

Clathrin

97

Vesicle membrane is linked to clathrin endocytic machinery via:

adaptor proteins

98

What happens to vesicles that are not recycled?

They are depleted

99

2 pathways recycled vesicle membrane can take:

direct or indirect (back to membrane or to ER)

100

Nicotinic receptor is AKA:

ionotropic

101

This type of cholinergic receptor directly activates an ion channel:

nicotinic ionotropic

102

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

muscarinic metabotropic

103

This type of cholinergic receptor is located in the NMJ:

nicotinic ionotropic

104

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

nicotinic ionotropic

105

Are nicotinic receptors ionotropic or metabotropic?

ionotropic

106

Are muscarinic receptors ionotropic or metabotropic?

metabotropic

107

This type of receptor can only activate GpCoupled intracellular signaling:

muscarinic metabotropic

108

how do muscarinic metabotropic receptors affect conductance of many channels?

via intracellular signalling

109

This type of receptor is located at neuroeffector junctions:

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

110

Agents that activate receptors:

agonists

111

T or F? succinylcholine is hydrolyzed by AChE:

F.

112

Prolonged exposure to an agonist leads to:

desensitization

113

These can bind but can't activate receptors:

antagonist

114

Agonists and antagonists compete by:

mass action for binding the same receptor

115

Toxins blocking neuromuscular transmission:

botulinum toxin and alpha-bungarotoxin

116

botulinum toxin blocks:

exocytosis of vesicles

117

alpha-bungarotoxin blocks:

activation by ACh

118

How does botulinum toxin block exocytosis of vesicles?

proteolytically cleaving components of vesicle fusion machinery in presynaptic terminals

119

How does alpha-bungarotoxin block activation by ACh?

a small basic peptide binds AChR irreversible

120

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

botulinum toxin

121

botulinum toxin is produced by:

Clostridium botuminum

122

alpha-bungarotoxin is produced by:

banded krait snake, Bungarus multicinctus

123

Focal intoxication with botulinum toxin produces:

a chronic denervated state

124

This toxin works postsynaptically:

alpha-bungarotoxin

125

This toxin works presynaptically:

botulinum toxin

126

This toxin is a receptor agonist:

alpha-bungarotoxin

127

This is an autoimmune postsynaptic disease that impairs NM transmission:

myasthenia gravis

128

Effect of myasthenia gravis:

muscle weakness

129

2 diseases of the neuromuscular junction:

myasthemia gravis and Lambert-Eaton myasthenic syndrome

130

Autoantibodies against AChRs cause:

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

131

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

safety margin

132

Why does myasthenia gravis lead to muscle weakness?

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

133

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

F. decrease

134

What do autoantibodies block?

postsynaptic receptors

135

Do nicotinic receptor desensitizes quickly or slowly?

quickly

136

This is autoimmune presynaptic disease that impairs NM transmission:

Lambert-Eaton myasthenic syndrome

137

This NM disease is presynaptic while this is one postsynaptic:

Lambert-Eaton myasthenic syndrome, myasthenia gravis

138

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

Lambert-Eaton myasthenic syndrome

139

In Lambert-Eaton myasthenic syndrome autoantibodies are against:

specific class of Ca2+ channel

140

The only 2 agents that are excitatory at the NMJ:

ACh and nicotine

141

Effect of tetra toxin:

block nerve AP

142

Affect of bungarotoxin:

impair transmission

143

Affect of blocking AChE:

prolong the action of ACh