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Brain and Behavior > SDL: transmission I and II > Flashcards

SDL: transmission I and II Flashcards

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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
Q

what type of NTs undergo terminal synthesis?

A

small molecules like acetylcholine, norepinephrine

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26
Q

what type of NTs undergo somatic synthesis?

A

peptide neurotransmitters (like opioid peptides) are made in soma, then transported to the nerve terminal

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27
Q

what is the function of autoreceptors? where are they located?

A

on the presynaptic membrane, autoreceptors may bind NTs to modulate further release or uptake of the NT

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28
Q

action potential-dependent release of synaptic vesicle contents into the synaptic cleft happens in this order

A

depolarization, which leads to Ca2+ influx at the nerve terminal, which leads to exocytosis of the vesicles

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29
Q

3 characteristics of NT binding to postsynaptic receptor

A
  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)
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30
Q

enzyme that degrades acetylcholine

A

acetylcholine esterase (AChE)

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31
Q

ways that NT action can be terminated

A
  1. extracellular degradative enzymes 2. specific reuptake proteins 3. diffusion of NT away 4. internalization of ligand-receptor complex
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32
Q

transport of NT precursors into the nerve nerminal is usually active or passive process?

A

active

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33
Q

order of events in NT synthesis, release, action, inactivation

A

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.

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34
Q

to terminate activity of NT, the released NTs must be..

A

taken up by presynaptic terminal, diffused away, or metabolized

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35
Q

enzyme required to form acetyl choline

A

choline acetyl transferase

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36
Q

2 major classes of post-synaptic receptors

A

ionotropic, metabotropic

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37
Q

which type of post-synaptic receptor is ligand-gated?

A

ionotropic e.g. ACh nicotinic receptor

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38
Q

which type of post-synaptic receptor is an ion channel?

A

ionotropic

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39
Q

which type of post-synaptic receptor is a GPCR?

A

metabotropic

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40
Q

this type of post synaptic receptor is linked to an ion channel with help of G protein

A

GPCR, e.g. ACh muscarinic receptor

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41
Q

muscarinic receptor refers to..

A

parasympathetic effects

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42
Q

nicotinic receptor refers to..

A

autonomic stimulation

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43
Q

onset of effects mediated by ionotropic vs. metabotropic receptor

A

ionotropic is fast, metabotropic is slow

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44
Q

duration of effects mediated by ionotropic vs. metabotropic receptor

A

ionotropic is short, metabotropic is long

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45
Q

which is an ion channel itself, ionotropic or metabotropic?

A

ionotropic

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46
Q

which has a direct effect on the channel, ionotropic or metabotropic?

A

ionotropic

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47
Q

which acts as a second messenger, ionotropic or metabotropic?

A

metabotropic

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48
Q

which possesses the ability to amplify, ionotropic or metabotropic?

A

metabotropic

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49
Q

excitation or inhibition is determined by the _____ and not the _____

A

receptor, not the NT being released

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50
Q

an excitatory NT causes ____ of the membrane potential

A

depolarization, towards the firing threshold.

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51
Q

an inhibitory NT causes ____ of the membrane potential

A

hyperpolarization, away from the firing threashold

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52
Q

too much excitation results in..

A

epilepsy

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53
Q

too much inhibition results in..

A

coma, anesthesia

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54
Q

regulatory mechanisms that maintain proper balance between inhibition and excitation of neurons

A

presynaptic receptors, second messengers, feedback inhibition, presynaptic inhibition (axoaxonic synapses)

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55
Q

examples of amine NTs

A

ACh, dopamine, norepi, epi, serotonin, histamine

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56
Q

examples of amino acid NTs

A

glutamate, GABA, glycine

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57
Q

examples of neuropeptide NTs

A

opiod peptides

58
Q

examples of gas NTs

A

nitric oxide

59
Q

similarities between classical and peptide NTs

A

both bind to specific receptors, both are released from vesicles in a Ca2+ dependent manner.

60
Q

how are peptide NTs synthesized?

A

synthesis is directed by mRNA

61
Q

peptide precursors usually exist as ..

A

inactive precursor proteins first

62
Q

where are peptide NTs made

A

in the cell body and transported to the axonal terminal (instead of made in the terminal)

63
Q

how do peptide NTs become active?

A

during transport, they’re cut into smaller pieces because of peptidase activity, become active after this process

64
Q

the acetylcholine receptors

A

nicotinic, muscarinic

65
Q

the dopamine receptors

A

D2, D1 both inhibitory

66
Q

the norepi and epi receptors

A

alpha, beta

67
Q

receptors for serotonin

A

many receptors

68
Q

receptors for histamine

A

H1, H2

69
Q

glutamate receptors + are they ionotropic, metabotropic?

A

NMDA (ionotropic), and the other one is metabotropic

70
Q

GABA receptors + are they ionotropic or metabotropic?

A

GABAa (ionotropic); GABAb (metabotropic)

71
Q

which GABA receptor has a quick onset of action?

A

GABAa (ionotropic)

72
Q

opioid peptides

A

beta-endorphin, enkephalin, dynorphin

73
Q

pituitary peptides

A

oxytocin, vasopressin

74
Q

where is dynorphin synthesized?

A

in the cell body and transported to the axon terminal; usually exists as an inactive precursor.

75
Q

catecholamines are derived from..

A

tyrosine

76
Q

rate limiting enzyme of catecholamine synthesis?

A

tyrosine hydroxylase (puts the second hydroxyl group on the benzene ring of tyrosine, making it a “catechol”

77
Q

cold medicines mimic activation of..

A

sympathetic nervous system; call them sympathomimetics

78
Q

precursor of serotonin

A

tryptophan

79
Q

Zoloft and anti-anxiety meds are..

A

selective serotonin reuptake inhibitors (SSRIs), they allow serotonin to remain active longer

80
Q

precursor of histamine

A

histidine

81
Q

precursor of acetylcholine

A

choline

82
Q

rate-limiting step of ACh synthesis

A

uptake of choline

83
Q

biosynthetic enzyme of acetylcholine

A

choline acetyl transferase (CAT)

84
Q

ACh nicotinic receptor; where are these found?

A

ionotropic; found in a neuromuscular junction

85
Q

ACh muscarinic receptor

A

metabotropic

86
Q

where is acetylcholine esterase located?

A

extracellularly in the synaptic cleft

87
Q

is acetylcholine an excitatory or inhibitory transmitter?

A

it depends what receptor it binds to (N is excitatory, M is excitatory or inhibitory)

88
Q

are nicotinic receptors located on the neuron or the muscle cell?

A

muscle cell

89
Q

what does myasthenia gravis have to do with ACh nicotinic receptors?

A

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
Q

what does Lambert-Eaton syndrome cause?

A

produces antibodies against the Ca2+ channels in the presynaptic terminals that interfere with NT relase

91
Q

glutamate is considered this type of NT because all of its receptors lead to depolarization

A

excitatory

92
Q

precursor of glutamate

A

glutamine

93
Q

after glutamate function is completed..

A

glutamate is taken up by axon terminals and recycled

94
Q

ionotropic glutamate receptor

A

NMDA, non-NMDA

95
Q

effect of metabotropic receptor of glutamate

A

IP3, diacylglycerol are released after the receptor is activated

96
Q

what is the NMDA glutamate receptor important for?

A

learning and memory

97
Q

the NMDA ionotropic glutamate receptor requires co-activation of the..

A

glycine binding site

98
Q

ligand-binding of NMDA ionotropic glutamate receptor causes opening of.

A

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
Q

excessive glutamate release during stroke and CNS trauma can lead to neuronal death; this is a type of _____

A

excitotoxicity

100
Q

precursor of GABA

A

glutamate

101
Q

type of NT that GABA is considered to be; why?

A

inhibitory because all receptors lead to hyperpolarization

102
Q

the GABAa ionotropic receptor causes

A

Cl- influx, thus hyperpolarization

103
Q

the GABAb metabotropic receptor causes

A

K+ efflux, thus hyperpolarization

104
Q

glycine is considered this type of NT because activation of its receptors leads to..

A

inhibitory NT; activation of its receptor leads to hyperpolarization

105
Q

what mechanism does glycine receptor activation lead to hyperpolarization?

A

influx of Cl-

106
Q

T/F: glutamate is an inhibitory transmitter

A

false; its excitatory (depolarization)

107
Q

T/F: GABA is an inhibitory NT

A

true

108
Q

T/F: ACh is an excitatory NT

A

it depends: nicotinic receptor is excitatory; muscarinic can be excitatory or inhibitory

109
Q

T/F: glycine is an excitatory NT

A

false; glycine is an inhibitory NT

110
Q

T/F: activation of ionotropic receptor always causes excitation

A

false; ionotropic receptors can be excitatory (nicotinic) or inhibitory (GABAa)

111
Q

T/F: activation of metabotropic receptor always causes excitation

A

false; metabotropic can be excitatory (glutamate) or inhibitory (GABAb)

112
Q

areas of conc of ACh

A

neuromuscular, autonomic, parasympathetic

113
Q

areas of conc of norepi

A

sympathetic

114
Q

*areas of conc of glycine

A

spinal cord (major inhibitory NT in the spinal cord is glycine)

115
Q

responsible for runner’s high

A

beta-endorphin (opiod peptide)

116
Q

mammalian neutopeptides

A

growth hormone releasing hormone, coricotropin, oxytocin, insulin, cholecystokinin, beta-endorphin, epidermal growth factor

117
Q

which NT acts as a retrograde messenger (going from postsynaptic to presynaptic cell?)

A

nitric oxide

118
Q

in the periphery, NO causes what type of muscle to relax, resulting in dilation

A

smooth muscle

119
Q

drug that contains NO

A

viagra

120
Q

an agonist does what to surface receptors

A

activates

121
Q

an antagonist does what to surface receptors

A

blocks them

122
Q

blocks binding of acetylcholine to its nicotinic receptor in the neuromuscular jucntion

A

alpha-bungarotoxin (snake venom)

123
Q

drug that increases the FREQUENCY of GABAa Cl- channel opening

A

benzodiazepine (valium)

124
Q

valium causes a neuron to become..

A

hyperpolarized

125
Q

drug that causes blockade of release of ACh from the nerve terminal

A

botulinum toxin

126
Q

under what conditions do we see botulinum toxin in food?

A

some improperly canned/preserved foods; also some c. botulinum spores can be found in honey and cause infantile botulism

127
Q

compound that irreversibly inactivates acetylcholinesterase, i.e. blocking degradative enzyme

A

organophosphates (insecticides)

128
Q

muscarinic receptor blocker

A

atropine

129
Q

GABAb receptor antagonist

A

baclofen (for epilepsy)

130
Q

increase duration of GABAa Cl- channel opneing

A

barbiturate/phenobarbital

131
Q

blocks monoamine reuptake at synapse to prolong action of NTs

A

cocaine

132
Q

blocks binding of ACh to its N receptor on skeletal muscle

A

curare

133
Q

agonist at postsynaptic serotonin receptors

A

LSD

134
Q

mimics binding of opioid peptodes to produce analgesia

A

morphine

135
Q

inhibit AChE activity prololonging ACh activity

A

neostigmine

136
Q

a NMDA glutamate receptor blocker

A

phencyclidine (PCP, angel dust)

137
Q

glycine receptor blocker (in rat poison)

A

strychnine

138
Q

block monoamine reuptake

A

tricyclic antidepressants

139
Q

selective serotonin reuptake

A

zoloft

140
Q

what are the unique properties of NMDA glutamate receptor?

A

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
Q

does the thymus play a role in myasthenia gravis?

A

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

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