SDL: transmission I and II Flashcards

1
Q

what type of cell produces myelin in the peripheral nervous system?

A

Schwann cells

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2
Q

What type of cell produces myelin in the CNS?

A

oligodendrocyte (a type of glial cell)

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3
Q

where a neuron receives inputs from many other neurons

A

convergence of inputs

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4
Q

types of synapses

A

axodendritic, axosomatic, dendrodendritic, axoaxonic

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5
Q

what is the function of the axon hillock?

A

the last site in the soma where membrane potentials propagated from synaptic inputs are summated before being transmitted to the axon

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6
Q

where synaptic vesicles aggregate before release

A

presynaptic density

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7
Q

these function to terminate the activity of a neurotransmitter

A

degradative enzymes

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8
Q

where the receptors aggregate

A

postsynaptic density

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9
Q

which achieves better control over excitatory OR inhibitory synapses: chemical or electrical transmission?

A

chemical transmission

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10
Q

3 characteristics of electrical junctions

A
  1. uses gap junctions 2. bidirectional communication 3. faster than chemical synapses
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11
Q

3 characteristics of chemical transmission

A
  1. uses a chemical synapse 2. unidirectional communication 3. relatively slow
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12
Q

most neurons in the mammalian CNS use this type of transmission to communicate with one another.

A

chemical transmission

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13
Q

what are the 4 criteria of a neurotransmitter?

A

localization, release, mimicry, inactivation

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14
Q

describe “localization” to establish a substance as a neurotransmitter

A

it is present at the nerve terminal

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15
Q

describe “release” to establish a substance as a NT

A

it is released after an action potential reaches the nerve terminal

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16
Q

describe “mimicry’ to establish a substance as a NT

A

once its structure is identified, should be able to synthesize the compound, apply it to a post-syn cell, and observe the same response as from the native NT

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17
Q

describe “inactivation” to establish a substance as a NT

A

the neurotransmitter should be inactivated by a specific mechanism, e.g. by enzymatic rxn

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18
Q

examples of some NT that do not fit the criteria

A

nitric oxide , dynorphin (peptide)

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19
Q

what do the structures of dopamine, epi, and norepi all have in common?

A

a substituted 1, 2-dihydroxy benzene ring

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20
Q

dopamine, epi, and norepi are all derived from..

A

tyrosine, which must first be hydroxylated

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21
Q

enzymatic control of NT synthesis can be increased by..

A

increasing the synthesis of the enzyme molecules (relatively slow process)

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22
Q

activity of enzymes that produce NTs can be altered (increased/decreased) by..

A

phosphorylation (relatively fast)

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23
Q

what determines the overall speed of synthesis of NTs?

A

the rate-limiting step (usually the 1st enzyme in the pathway)

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24
Q

describe specificity of enzymatic control of NT synthesis

A

presence or absence of relevant synthetic enzymes e.g. need choline acetyltransferase (CAT) to make acetylcholine

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25
what type of NTs undergo terminal synthesis?
small molecules like acetylcholine, norepinephrine
26
what type of NTs undergo somatic synthesis?
peptide neurotransmitters (like opioid peptides) are made in soma, then transported to the nerve terminal
27
what is the function of autoreceptors? where are they located?
on the presynaptic membrane, autoreceptors may bind NTs to modulate further release or uptake of the NT
28
action potential-dependent release of synaptic vesicle contents into the synaptic cleft happens in this order
depolarization, which leads to Ca2+ influx at the nerve terminal, which leads to exocytosis of the vesicles
29
3 characteristics of NT binding to postsynaptic receptor
1. single NT may bind to mult types of receptors 2. binding is usually reversible 3. effect is conc. dependent i.e. low conc can activate specific receptors, high conc. can bind specific and non-specific receptors (can be undesirable)
30
enzyme that degrades acetylcholine
acetylcholine esterase (AChE)
31
ways that NT action can be terminated
1. extracellular degradative enzymes 2. specific reuptake proteins 3. diffusion of NT away 4. internalization of ligand-receptor complex
32
transport of NT precursors into the nerve nerminal is usually active or passive process?
active
33
order of events in NT synthesis, release, action, inactivation
transport of precursors into the nerve terminal, precursors undergo enzymatic changes, NT is stored, action potential causes Ca2+ influx, vesicles are released, receptor binding, response to NT, then either reuptake, diffusion away, or autoreceptor binding occurs.
34
to terminate activity of NT, the released NTs must be..
taken up by presynaptic terminal, diffused away, or metabolized
35
enzyme required to form acetyl choline
choline acetyl transferase
36
2 major classes of post-synaptic receptors
ionotropic, metabotropic
37
which type of post-synaptic receptor is ligand-gated?
ionotropic e.g. ACh nicotinic receptor
38
which type of post-synaptic receptor is an ion channel?
ionotropic
39
which type of post-synaptic receptor is a GPCR?
metabotropic
40
this type of post synaptic receptor is linked to an ion channel with help of G protein
GPCR, e.g. ACh muscarinic receptor
41
muscarinic receptor refers to..
parasympathetic effects
42
nicotinic receptor refers to..
autonomic stimulation
43
onset of effects mediated by ionotropic vs. metabotropic receptor
ionotropic is fast, metabotropic is slow
44
duration of effects mediated by ionotropic vs. metabotropic receptor
ionotropic is short, metabotropic is long
45
which is an ion channel itself, ionotropic or metabotropic?
ionotropic
46
which has a direct effect on the channel, ionotropic or metabotropic?
ionotropic
47
which acts as a second messenger, ionotropic or metabotropic?
metabotropic
48
which possesses the ability to amplify, ionotropic or metabotropic?
metabotropic
49
excitation or inhibition is determined by the _____ and not the _____
receptor, not the NT being released
50
an excitatory NT causes ____ of the membrane potential
depolarization, towards the firing threshold.
51
an inhibitory NT causes ____ of the membrane potential
hyperpolarization, away from the firing threashold
52
too much excitation results in..
epilepsy
53
too much inhibition results in..
coma, anesthesia
54
regulatory mechanisms that maintain proper balance between inhibition and excitation of neurons
presynaptic receptors, second messengers, feedback inhibition, presynaptic inhibition (axoaxonic synapses)
55
examples of amine NTs
ACh, dopamine, norepi, epi, serotonin, histamine
56
examples of amino acid NTs
glutamate, GABA, glycine
57
examples of neuropeptide NTs
opiod peptides
58
examples of gas NTs
nitric oxide
59
similarities between classical and peptide NTs
both bind to specific receptors, both are released from vesicles in a Ca2+ dependent manner.
60
how are peptide NTs synthesized?
synthesis is directed by mRNA
61
peptide precursors usually exist as ..
inactive precursor proteins first
62
where are peptide NTs made
in the cell body and transported to the axonal terminal (instead of made in the terminal)
63
how do peptide NTs become active?
during transport, they're cut into smaller pieces because of peptidase activity, become active after this process
64
the acetylcholine receptors
nicotinic, muscarinic
65
the dopamine receptors
D2, D1 both inhibitory
66
the norepi and epi receptors
alpha, beta
67
receptors for serotonin
many receptors
68
receptors for histamine
H1, H2
69
glutamate receptors + are they ionotropic, metabotropic?
NMDA (ionotropic), and the other one is metabotropic
70
GABA receptors + are they ionotropic or metabotropic?
GABAa (ionotropic); GABAb (metabotropic)
71
which GABA receptor has a quick onset of action?
GABAa (ionotropic)
72
opioid peptides
beta-endorphin, enkephalin, dynorphin
73
pituitary peptides
oxytocin, vasopressin
74
where is dynorphin synthesized?
in the cell body and transported to the axon terminal; usually exists as an inactive precursor.
75
catecholamines are derived from..
tyrosine
76
rate limiting enzyme of catecholamine synthesis?
tyrosine hydroxylase (puts the second hydroxyl group on the benzene ring of tyrosine, making it a "catechol"
77
cold medicines mimic activation of..
sympathetic nervous system; call them sympathomimetics
78
precursor of serotonin
tryptophan
79
Zoloft and anti-anxiety meds are..
selective serotonin reuptake inhibitors (SSRIs), they allow serotonin to remain active longer
80
precursor of histamine
histidine
81
precursor of acetylcholine
choline
82
rate-limiting step of ACh synthesis
uptake of choline
83
biosynthetic enzyme of acetylcholine
choline acetyl transferase (CAT)
84
ACh nicotinic receptor; where are these found?
ionotropic; found in a neuromuscular junction
85
ACh muscarinic receptor
metabotropic
86
where is acetylcholine esterase located?
extracellularly in the synaptic cleft
87
is acetylcholine an excitatory or inhibitory transmitter?
it depends what receptor it binds to (N is excitatory, M is excitatory or inhibitory)
88
are nicotinic receptors located on the neuron or the muscle cell?
muscle cell
89
what does myasthenia gravis have to do with ACh nicotinic receptors?
autoimmune disease that produces antibodies against the post-synaptic ACh receptor, causing reduced responsiveness of the muscle to the activity of the motor neurons
90
what does Lambert-Eaton syndrome cause?
produces antibodies against the Ca2+ channels in the presynaptic terminals that interfere with NT relase
91
glutamate is considered this type of NT because all of its receptors lead to depolarization
excitatory
92
precursor of glutamate
glutamine
93
after glutamate function is completed..
glutamate is taken up by axon terminals and recycled
94
ionotropic glutamate receptor
NMDA, non-NMDA
95
effect of metabotropic receptor of glutamate
IP3, diacylglycerol are released after the receptor is activated
96
what is the NMDA glutamate receptor important for?
learning and memory
97
the NMDA ionotropic glutamate receptor requires co-activation of the..
glycine binding site
98
ligand-binding of NMDA ionotropic glutamate receptor causes opening of.
non-specific cation conducting channel i.e. calcium influx can lead to generation of NO (2nd messenger effect although the ionotropic receptors are not true second messengers)
99
excessive glutamate release during stroke and CNS trauma can lead to neuronal death; this is a type of _____
excitotoxicity
100
precursor of GABA
glutamate
101
type of NT that GABA is considered to be; why?
inhibitory because all receptors lead to hyperpolarization
102
the GABAa ionotropic receptor causes
Cl- influx, thus hyperpolarization
103
the GABAb metabotropic receptor causes
K+ efflux, thus hyperpolarization
104
glycine is considered this type of NT because activation of its receptors leads to..
inhibitory NT; activation of its receptor leads to hyperpolarization
105
what mechanism does glycine receptor activation lead to hyperpolarization?
influx of Cl-
106
T/F: glutamate is an inhibitory transmitter
false; its excitatory (depolarization)
107
T/F: GABA is an inhibitory NT
true
108
T/F: ACh is an excitatory NT
it depends: nicotinic receptor is excitatory; muscarinic can be excitatory or inhibitory
109
T/F: glycine is an excitatory NT
false; glycine is an inhibitory NT
110
T/F: activation of ionotropic receptor always causes excitation
false; ionotropic receptors can be excitatory (nicotinic) or inhibitory (GABAa)
111
T/F: activation of metabotropic receptor always causes excitation
false; metabotropic can be excitatory (glutamate) or inhibitory (GABAb)
112
areas of conc of ACh
neuromuscular, autonomic, parasympathetic
113
areas of conc of norepi
sympathetic
114
*areas of conc of glycine
spinal cord (***major inhibitory NT in the spinal cord is glycine)***
115
responsible for runner's high
beta-endorphin (opiod peptide)
116
mammalian neutopeptides
growth hormone releasing hormone, coricotropin, oxytocin, insulin, cholecystokinin, beta-endorphin, epidermal growth factor
117
which NT acts as a retrograde messenger (going from postsynaptic to presynaptic cell?)
nitric oxide
118
in the periphery, NO causes what type of muscle to relax, resulting in dilation
smooth muscle
119
drug that contains NO
viagra
120
an agonist does what to surface receptors
activates
121
an antagonist does what to surface receptors
blocks them
122
blocks binding of acetylcholine to its nicotinic receptor in the neuromuscular jucntion
alpha-bungarotoxin (snake venom)
123
drug that increases the FREQUENCY of GABAa Cl- channel opening
benzodiazepine (valium)
124
valium causes a neuron to become..
hyperpolarized
125
drug that causes blockade of release of ACh from the nerve terminal
botulinum toxin
126
under what conditions do we see botulinum toxin in food?
some improperly canned/preserved foods; also some c. botulinum spores can be found in honey and cause infantile botulism
127
compound that irreversibly inactivates acetylcholinesterase, i.e. blocking degradative enzyme
organophosphates (insecticides)
128
muscarinic receptor blocker
atropine
129
GABAb receptor antagonist
baclofen (for epilepsy)
130
increase duration of GABAa Cl- channel opneing
barbiturate/phenobarbital
131
blocks monoamine reuptake at synapse to prolong action of NTs
cocaine
132
blocks binding of ACh to its N receptor on skeletal muscle
curare
133
agonist at postsynaptic serotonin receptors
LSD
134
mimics binding of opioid peptodes to produce analgesia
morphine
135
inhibit AChE activity prololonging ACh activity
neostigmine
136
a NMDA glutamate receptor blocker
phencyclidine (PCP, angel dust)
137
glycine receptor blocker (in rat poison)
strychnine
138
block monoamine reuptake
tricyclic antidepressants
139
selective serotonin reuptake
zoloft
140
what are the unique properties of NMDA glutamate receptor?
ionotropic opening of channels, can permit Ca2+ influx if membrane is depolarized (can act as a 2nd messenger, which is unusual for normal ionotropic receptors)
141
does the thymus play a role in myasthenia gravis?
yes, it remains large and abnormal in adults with the disease, and scientists think that it may send incorrect messages to the immune system to develop antibodies against the ACh post synaptic receptor