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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
Q

somatodendritic autoreceptor

A

autoreceptors on cell bodies/dendrites that slow firing and reduce transmitter release

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26
Q

how would transmitter release be affected when autoreceptors are stimulated

A

reduce transmitter release

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27
Q

what are the 3 main ways that transmitters are removed from the synapse?

A

enzymatic degradation
reuptake by presynapse
reuptake by glial cells

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28
Q

transoirter proteins definition

A

use active transport to mediate reuptake

29
Q

true or false; autoreceptors directly effect transporter proteins function

A

false, their functions are unrelated

30
Q

true or false; NT’s have one type of receptor they bind to

A

false, NT’s have a few receptor subtypes that can have different cellular effects

31
Q

what are the two ways that G proteins act

A

inhibit/activate ion channels
stimulate/inhibit effector enzymes to synthesize/breakdown second messengers

32
Q

what residues do G proteins bind to?

A

guanine

33
Q

what do second messengers do?

A

are inside the cell and activate protein kinases that phosphorylate other proteins

34
Q

what can phosphorylation of ion channels/receptors do?

A

change their function

35
Q

what can phosphorylation of nuclear proteins do?

A

turn gene expression on/off

36
Q

what does cAMP stand for

A

Cyclic adenosine monophosphate

37
Q

what are two common second messenger pathways

A

cAMP
Phosphoinositide

38
Q

what is the cAMP pathway and what NTs control it

A

stimulates protein kinase A and controlled by dopamine, norepinephrine, serotonin, and endorphins

39
Q

what is the phosphoinositide pathway? what NTs is it controlled by?

A

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
Q

what does DAG stand for

A

diacylglycerol

41
Q

what does IP3 stand for

A

inositol trisphosphate

42
Q

what are the 11 primary ways a drug affects neural transmission?

A

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
Q

how is neural transmission affected when a drug acts as a precursor

A

increases rate of synthesis and activity by acting as the base for making the transmitter

44
Q

examples of precursors for dopamine and 5-HT

A

L-DOPA
Tryptophan

45
Q

how is neural transmission affected when a drug inhibits synthesis

A

blocks synthesis by targetting enzymes in the terminal that prevents it from creating more NT
more long term

46
Q

two drugs that inhibit transmitter synthesis

A

AMPT- inhibits tyrosine hydroxylase to make DA and NE
para-chlorophenylalanine; inhibits tryptophan hydroxylase to amke 5-HT

47
Q

how is neural transmission affected when a drug blocks storage in vesicles

A

transmission reduces because NT is exposed to degradation enzymes

48
Q

example of drug that disrupts DA, NE, and 5-HT vesicles and how

A

reserpine; blocks vesicular transporters

49
Q

how is neural transmission affected when a drug reverses uptake transporters?

A

stimulates the release

50
Q

two drugs that reverse uptake transporters

A

D-Amphetamine (Adderal); releases DA and NE
pseudoepherine (decongestant); like amphetamine, focuses more on NE

51
Q

example of drug that blocks Ach release and how

A

botulinum toxin (botox); does not allow synaptic vesicle to ‘hold hands’ with presynaptic membrane

52
Q

example of agonist drug that stimulates postsynapse receptors

A

heroin stimulates u-opioid receptor

53
Q

example of antagonist drugs that blocks postsynapse receptors

A

caffeine- adenosine receptors
atropine- Ach muscarinic receptors

54
Q

example of agonist drugs that stimulate autoreceptors

A

clonidine (NE)
8-OH-DPAT (5-HT)

55
Q

how is neural transmission affected by drugs that affect autoreceptors?

A

agonists will reduce transmitter release
antagonist is vice versa

56
Q

example of antagonist drugs that block autoreceptors

A

Yohimbine (NE)
pindolol (5-HT)

57
Q

example of drugs that blocks the enzyme for NT breakdown

A

physostigmine (block Ach enzyme)
phenelzine (block NE, DA, 5HT enzyme)

58
Q

what does physostigmine do

A

block acetyl-cholinesterase that breaks down Ach

59
Q

what does phenelzine do

A

blocks monoamine oxidase that breaks down DA, NE and 5-HT

60
Q

how is neural transmission affected by drugs that block enzymes for NT breakdown?

A

enhances NT action

61
Q

how is neural transmission affected by drugs that block uptake transporters?

A

enhances NT action

62
Q

example of two drugs that block uptake transporters?

A

cocaine
tricyclic antidepressants

63
Q

what does cocaine do

A

block monoamine uptake transporters (DA, 5-HT, NE)

64
Q

what does tricyclic antidepressants do

A

block NE uptake transporters

65
Q

what pimarily removes Ach?

A

enzymatic breakdown

66
Q

allosteric sites

A

additional binding site on a receptor

67
Q

allosteric modulators

A

molecules that bind to allosteric sites and alter receptor functioning by changing its conformation

68
Q

how do allosteric modulators affect receptor signalling

A

positive or negative allosteric modulators change effect of the agonist
no effect of their own

PSYC 462 (11 decks)

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