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PSYC 462 > Ch. 3 Chemical SIignalling By NeuroTransmitters > Flashcards

Ch. 3 Chemical SIignalling By NeuroTransmitters Flashcards

1
Q

what are the three major types of synapses

A

axodendritic
axosomatic
axoaxonic

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2
Q

axodendritic definition

A

terminal connects with a dendrite of the postsynpatic cell
most common

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3
Q

axosomatic definition

A

axon terminal forms connection with neuron cell body

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4
Q

axoaxonic definition

A

axon synapsing on another axon terminal
must be heteroreceptors

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5
Q

what is presynaptic inhibition

A

reducing transmitter release of the receiving terminal of axoaxonic synapse

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6
Q

what is presynaptic facilitation

A

enhancing transmitter release of the receiving terminal of axoaxonic synapse

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7
Q

heteroreceptor definition

A

receptor on axon terminal that responds to differnet NT from those released by the other terminal in an axoaxonic connection

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8
Q

what determines degree of depolarization in synaptic connections

A

a synaptic connection closer to the cell body will have a stronger/ more polarizing effect

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9
Q

classical neurotransmitters

A

single molecule transmitters
amino acids
monoamines
aceylcholine

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10
Q

types of monoamines

A

dopamine
norepinephrine
serotonin

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11
Q

types of amino acid NTs

A

glutamate
GABA

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12
Q

nonclassical neurotrasmitters

A

transmitters that are not just a single molecule
neuropeptides
lipids

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13
Q

true or false, individual neurons can only make one type of NT

A

false, it could make several

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14
Q

which transmitters are the only ones not made in the terminals, but in the soma?

A

peptides

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15
Q

10 steps of neurotransmission

A
  1. NT synthesis/storage
  2. AP comes in presynapse
  3. depolarization opens Ca+2 channels
  4. Ca enters
  5. Ca causes vesicles to fuse with presynaptic membrane
  6. NT release in cleft from exocytosis
  7. NTs bind to postsynapse receptors
  8. receptors react
  9. postsynapse excites of inhibits
  10. vesicle membrane gets recycled via endocytosis
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16
Q

neuromodulators definition

A

will enhance, reduce, or prolong the action of a neurotransmitter

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17
Q

true or false: neuromodulators are not easily defined as ‘excitatory’ or ‘inhibitory’ because that depends on many factors

A

true

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18
Q

volume transmission

A

non-localized release of a ‘mist’ of transmitter that can reach more axons and farther
mostly encounter extrasynaptic receptors

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19
Q

extrasynaptic receptors

A

receptors not tightly localized to the presynaptic terminal

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20
Q

true or false; neuromodulators and neurotransmitters are very distinct from each other

A

false, depends on the receptor they interact with

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21
Q

what releases more transmitter- evenly spaced firing or burst firing?

A

burst firing

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22
Q

in what context would we switch to burst firing in a synapse

A

when there is motivational or emotionally salient stimuli

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23
Q

autoreceptor definition

A

receptor that responds to the same NT being released by the presynapse and inhibits further release/firing

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24
Q

presynaptic terminal autoreceptor

A

when activated at the presynapse, inhibits further transmitter release

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25
somatodendritic autoreceptor
autoreceptors on cell bodies/dendrites that slow firing and reduce transmitter release
26
how would transmitter release be affected when autoreceptors are stimulated
reduce transmitter release
27
what are the 3 main ways that transmitters are removed from the synapse?
enzymatic degradation reuptake by presynapse reuptake by glial cells
28
transoirter proteins definition
use active transport to mediate reuptake
29
true or false; autoreceptors directly effect transporter proteins function
false, their functions are unrelated
30
true or false; NT's have one type of receptor they bind to
false, NT's have a few receptor subtypes that can have different cellular effects
31
what are the two ways that G proteins act
inhibit/activate ion channels stimulate/inhibit effector enzymes to synthesize/breakdown second messengers
32
what residues do G proteins bind to?
guanine
33
what do second messengers do?
are inside the cell and activate protein kinases that phosphorylate other proteins
34
what can phosphorylation of ion channels/receptors do?
change their function
35
what can phosphorylation of nuclear proteins do?
turn gene expression on/off
36
what does cAMP stand for
Cyclic adenosine monophosphate
37
what are two common second messenger pathways
cAMP Phosphoinositide
38
what is the cAMP pathway and what NTs control it
stimulates protein kinase A and controlled by dopamine, norepinephrine, serotonin, and endorphins
39
what is the phosphoinositide pathway? what NTs is it controlled by?
breaks down phospholipid in cell membrane and liberates two 2nd messengers; DAG and IP3 increases Ca in the postsynapse and activate protein kinase C controlled by Ach, NE, 5-HT
40
what does DAG stand for
diacylglycerol
41
what does IP3 stand for
inositol trisphosphate
42
what are the 11 primary ways a drug affects neural transmission?
act as precursor inhibit synthesis block storage in vesicles stimualte release by reversing uptake transporters block NT release stimulate/block postsynaptic receptor stimulate/block autoreceptor block enzymes for NT breakdown block reuptake transporters
43
how is neural transmission affected when a drug acts as a precursor
increases rate of synthesis and activity by acting as the base for making the transmitter
44
examples of precursors for dopamine and 5-HT
L-DOPA Tryptophan
45
how is neural transmission affected when a drug inhibits synthesis
blocks synthesis by targetting enzymes in the terminal that prevents it from creating more NT more long term
46
two drugs that inhibit transmitter synthesis
AMPT- inhibits tyrosine hydroxylase to make DA and NE para-chlorophenylalanine; inhibits tryptophan hydroxylase to amke 5-HT
47
how is neural transmission affected when a drug blocks storage in vesicles
transmission reduces because NT is exposed to degradation enzymes
48
example of drug that disrupts DA, NE, and 5-HT vesicles and how
reserpine; blocks vesicular transporters
49
how is neural transmission affected when a drug reverses uptake transporters?
stimulates the release
50
two drugs that reverse uptake transporters
D-Amphetamine (Adderal); releases DA and NE pseudoepherine (decongestant); like amphetamine, focuses more on NE
51
example of drug that blocks Ach release and how
botulinum toxin (botox); does not allow synaptic vesicle to 'hold hands' with presynaptic membrane
52
example of agonist drug that stimulates postsynapse receptors
heroin stimulates u-opioid receptor
53
example of antagonist drugs that blocks postsynapse receptors
caffeine- adenosine receptors atropine- Ach muscarinic receptors
54
example of agonist drugs that stimulate autoreceptors
clonidine (NE) 8-OH-DPAT (5-HT)
55
how is neural transmission affected by drugs that affect autoreceptors?
agonists will reduce transmitter release antagonist is vice versa
56
example of antagonist drugs that block autoreceptors
Yohimbine (NE) pindolol (5-HT)
57
example of drugs that blocks the enzyme for NT breakdown
physostigmine (block Ach enzyme) phenelzine (block NE, DA, 5HT enzyme)
58
what does physostigmine do
block acetyl-cholinesterase that breaks down Ach
59
what does phenelzine do
blocks monoamine oxidase that breaks down DA, NE and 5-HT
60
how is neural transmission affected by drugs that block enzymes for NT breakdown?
enhances NT action
61
how is neural transmission affected by drugs that block uptake transporters?
enhances NT action
62
example of two drugs that block uptake transporters?
cocaine tricyclic antidepressants
63
what does cocaine do
block monoamine uptake transporters (DA, 5-HT, NE)
64
what does tricyclic antidepressants do
block NE uptake transporters
65
what pimarily removes Ach?
enzymatic breakdown
66
allosteric sites
additional binding site on a receptor
67
allosteric modulators
molecules that bind to allosteric sites and alter receptor functioning by changing its conformation
68
how do allosteric modulators affect receptor signalling
positive or negative allosteric modulators change effect of the agonist no effect of their own

PSYC 462 (11 decks)

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