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B&B W1. E1 > Synaptic Trans SDL1 > Flashcards

Synaptic Trans SDL1 Flashcards

1
Q

Where synaptic vesicles aggregate before release

A

presynaptic density, active site

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2
Q

Where receptor aggregate

A

postsynaptic density

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3
Q

electrical junctions

A

gap junctions, bidirectional, fast

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4
Q

chemical transmission

A

chemical synapse, unidirectional, slow, better controlled

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5
Q

Criteria for NT

A

localization, release, mimicry, inactivation

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6
Q

Tyrosine Derivatives?

A

Epinephrine, Dopamine, Norepinephrine

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7
Q

NT synthesis and packaging

A

step- by-step from readily available precursors

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8
Q

Enzymatic Control of Synthesis

A

enzyme molecule concentration, rate limiting step, phosphorylation, specificity

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9
Q

where are peptide neurotransmitters made?

A

soma –> nerve terminal

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10
Q

where are small molecules made?

A

ACh, Epi made in nerve terminal

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11
Q

What do autoreceptors do?

A

bind NT and modulate release of transmitter

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12
Q

AP sequence?

A

Depolarization –> Ca2+ influx at terminal –> exocytosis of vesicle

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13
Q

Binding of NT to postsynaptic receptor (3)

A
  • single transmitter can bind multiple times
  • usually reversible
  • effect is concentration dependent
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14
Q

High concentration of NT may cause…

A

binding to specific and non-specific receptors –> undesirable side effects if non-specific activate

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15
Q

Termination of NT action (4)

A
  • extracellular degradation enzymes
  • specific reuptake proteins
  • diffusion of NT away
  • internalization of ligand-receptor complex
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16
Q

What are the two classes of postsynaptic receptors?

A

ionotropic and metabotropic

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17
Q

What is an ionotropic receptor?

A

ligand-gated, fast ex: ACh nicotinic

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18
Q

What is a metabotropic receptor?

A

G-protein coupled, slow ex: ACh muscarinic receptor

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19
Q

Characteristics of Ionotropic

A

fast onset, short duration, direct effect on channel, no second messenger or amplification

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20
Q

Characteristics of Metabotropic

A

slow onset, long duration, no ion channel, no direct effect on channel, second messenger and amplification

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21
Q

What determines excitation or inhibition?

A

receptor

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22
Q

Excitation

A

Depolarization, excitatory

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23
Q

Inhibition

A

Hyperpolarization, Inhibitory

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24
Q

Pre-synaptic inhibition

A

axo-axonic synapses

25
Q

too much excitation

A

epilepsey

26
Q

too much inhibition

A

anesthesia, coma

27
Q

4 types of NT

A

amines, amino acids, neuropeptides, gases

28
Q

Unique about Peptides

A
  • synthesis directed by mRNA
  • exist as inactive precursor
  • made in cell body–>terminal
  • cut into small pieces–> active
29
Q

Amines

A

Serotonin, Histamine, ACh, Dopamine, Epi, NE

SHADE N

30
Q

Amino Acids

A

Glutamate, GABA, Glycine

31
Q

Types of GABA

A

GABAa: ionotropic
GABAb: Metabotropic

32
Q

Neuropeptides

A

opioids, CCK, Oxytocin, Vasopressin

33
Q

Gases

A

NO, CO

34
Q

Opioid peptides

A

Beta-endorphin, enkephalin, dynorphin

35
Q

Catecholamines

A
  • dopamine, nor, epi
  • tyrosine derivatives
  • catechol nucleus
  • tyrosine hydroxylase is rate limiting
36
Q

Catecholamines and Cold medicine

A

mimic activation of sympathetic nervous system, reverse low BP

37
Q

Serotonin

A
  • Tyrptophan precursor
  • Zoloft, SSRI
  • allow serotonin to be active longer
38
Q

Histamine

A
  • histidine precursor

- cold medicines

39
Q

ACh

A
  • choline precursor
  • RL: uptake of choline
  • biosyn enzyme: CAT
  • muscarinic: metabotropic
  • degradative: AChE
40
Q

Glutamate

A
  • glutamine precursor
  • after, taken up by axon terminals
  • ionotropic: NMDA, non-NMDA
  • metabotropic: IP3, DAG
41
Q

What is glutamate considered as?

A

excitatory NT, too much release in stroke can lead to excitotoxicity

42
Q

GABA

A
  • glutamate precursor
  • iono: GABAa, Ca2+ influx
  • metab: GABAb, K+ efflux
43
Q

Glycine

A

considered inhibitory

44
Q

NO

A

gas, retrograde messenger, smooth muscle dilation

45
Q

α-bungarotoxin

A
  • snake venom

- blocks binding of ACh to nicotinic receptor in NM junction

46
Q

Benzodiazepine

A

tranqulizer, increases frequency of GABAa Cl- opening

47
Q

Zoloft

A

SSRI, block re-uptake

48
Q

Botox

A

prevents release of ACh from nerve terminal

49
Q

Organophosphates

A

irreversibly inactivates acetylcholinesterase

50
Q

atropine

A

muscarnic receptor blocker, block postganglionic PS

51
Q

Baclofen

A
  • GABAb agonist

- epilepsy

52
Q

Barbituate

A

sedative, increase duration of GABAa Cl- opening

53
Q

Cocaine

A

blocks monoamine re-uptake at synapse, prolong NT

54
Q

Curare

A
  • plant toxin

- blocks binding ACh to nicotinic on skeletal muscle

55
Q

Morphine

A

mimics opioid peptide binding

56
Q

Neostigmine

A
  • inhibit acetylcholinesterase, prolong ACh

- treats MS

57
Q

PCP

A

NMDA glutamate receptor blocker

58
Q

Strychnine

A
  • glycine receptor blocker

- rat poison

59
Q

tricyclic antidepressants

A

blocks monoamine reuptake

B&B W1. E1 (9 decks)

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