Lecture 5 Flashcards
1
Q
This type of synapse is separated by a Gap-junction channel:
A
electrical synapse
2
Q
This type of synapse is separated by a synaptic cleft:
A
chemical synapse
3
Q
Majority of synapses in the CNS and PNS are mediated by:
A
chemical synapse
4
Q
This type of synapse involves a presynaptic cell whereas this type involves a presynaptic cleft:
A
electrical, chemical
5
Q
This type of synapse is formed by hemichannels:
A
electrical (also called connexons)
6
Q
T or F? A synapse transmits intracellular signals.
A
F. Intercellular
7
Q
Intercellular signals can be either:
A
electrical or chemical
8
Q
These mediate electrical or electronic transmission:
A
gap junctions
9
Q
Gap junctions are generally (excitatory/inhibitory)
A
excitatory
10
Q
T or F? Chemical signals mediate only excitation.
A
F. either excitation or inhibition
11
Q
What type of channel does an AP open in the nerve terminal of a presynaptic cell?
A
Ca
12
Q
What causes vesicle fusion?
A
Ca entry
13
Q
What causes transmitter release?
A
Ca entry
14
Q
Wat type of channel does an AP open in the postsynaptic cell?
A
Na receptor-channels
15
Q
This type of channel is both receptor and channel:
A
Na
16
Q
How do currents from a presynaptic AP affect the postsynaptic PM?
A
they don’t, they are shunted in the synaptic cleft
17
Q
T or F? transmitter-receptor binding can produce a depolarization or hyperpolarization of the PM.
A
T
18
Q
This is a special synapse bw neuron and skeletal muscle:
A
NMJ
19
Q
Where is the cell body of the neuron located?
A
Spinal cord
20
Q
This is a ‘giant’ excitatory synapse:
A
NMJ
21
Q
What ensures high transmission reliability at the NMJ?
A
large size of synapse
22
Q
In the absence of disease, 1 nerve AP generates:
A
1 muscle AP
23
Q
Another name for NMJ
A
endplate potential
24
Q
Motor unit:
A
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
