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
too much excitation
epilepsey
26
too much inhibition
anesthesia, coma
27
4 types of NT
amines, amino acids, neuropeptides, gases
28
Unique about Peptides
- synthesis directed by mRNA - exist as inactive precursor - made in cell body-->terminal - cut into small pieces--> active
29
Amines
Serotonin, Histamine, ACh, Dopamine, Epi, NE | SHADE N
30
Amino Acids
Glutamate, GABA, Glycine
31
Types of GABA
GABAa: ionotropic GABAb: Metabotropic
32
Neuropeptides
opioids, CCK, Oxytocin, Vasopressin
33
Gases
NO, CO
34
Opioid peptides
Beta-endorphin, enkephalin, dynorphin
35
Catecholamines
- dopamine, nor, epi - tyrosine derivatives - catechol nucleus - tyrosine hydroxylase is rate limiting
36
Catecholamines and Cold medicine
mimic activation of sympathetic nervous system, reverse low BP
37
Serotonin
- Tyrptophan precursor - Zoloft, SSRI - allow serotonin to be active longer
38
Histamine
- histidine precursor | - cold medicines
39
ACh
- choline precursor - RL: uptake of choline - biosyn enzyme: CAT - muscarinic: metabotropic - degradative: AChE
40
Glutamate
- glutamine precursor - after, taken up by axon terminals - ionotropic: NMDA, non-NMDA - metabotropic: IP3, DAG
41
What is glutamate considered as?
excitatory NT, too much release in stroke can lead to excitotoxicity
42
GABA
- glutamate precursor - iono: GABAa, Ca2+ influx - metab: GABAb, K+ efflux
43
Glycine
considered inhibitory
44
NO
gas, retrograde messenger, smooth muscle dilation
45
α-bungarotoxin
- snake venom | - blocks binding of ACh to nicotinic receptor in NM junction
46
Benzodiazepine
tranqulizer, increases frequency of GABAa Cl- opening
47
Zoloft
SSRI, block re-uptake
48
Botox
prevents release of ACh from nerve terminal
49
Organophosphates
irreversibly inactivates acetylcholinesterase
50
atropine
muscarnic receptor blocker, block postganglionic PS
51
Baclofen
- GABAb agonist | - epilepsy
52
Barbituate
sedative, increase duration of GABAa Cl- opening
53
Cocaine
blocks monoamine re-uptake at synapse, prolong NT
54
Curare
- plant toxin | - blocks binding ACh to nicotinic on skeletal muscle
55
Morphine
mimics opioid peptide binding
56
Neostigmine
- inhibit acetylcholinesterase, prolong ACh | - treats MS
57
PCP
NMDA glutamate receptor blocker
58
Strychnine
- glycine receptor blocker | - rat poison
59
tricyclic antidepressants
blocks monoamine reuptake