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Sp. Phys 1 > 2. Synaptic Transmission and Neurotransmitters > Flashcards

2. Synaptic Transmission and Neurotransmitters Flashcards

1
Q

electrical synapse

A

2 neurons are connected by a gap junction which allows electrical current to flow directly from one cell to another

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2
Q

connexin

A

located on pre and post synaptic clefts with very small gap between

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3
Q

size of electrical synapse gap

A

3nm

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4
Q

gap junction

A

aggregates of intercellular channels that permit direct cell–cell transfer of ions and small molecules

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5
Q

types of ions/molecules that can pass through gap junction

A

Ca2+
IP3
cAMP
Na+
etc

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6
Q

Charcot-Marie-Tooth disease

A

affects sensory and motor nerves in arms, hands, legs, feet.

nerves degenerate and lose ability to communication with distant targets

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7
Q

Action Potential in CMT disease

A

decreased

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8
Q

CMT disease type

A

heterogenous genetic disease

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9
Q

CMTX1

A

2nd most common form of CMT
caused by x-linked mutations in a gene that provides instructions for making the protein connexin-32

connexin-32 is part of gap junction channels in myelinating schwann cells

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10
Q

chemical synapses

A

release neurotransmitters from presynaptic membrane and bind to its receptors on postsynaptic or presynaptic membrane

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11
Q

chemical synapse gap distance

A

30nm

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12
Q

where are VG Ca++ channels located?

A

presynaptic membrane

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13
Q

parts of a neural synapse

A

presynaptic terminal
postynaptic terminal
synapse
vesicle
neurotransmitters
receptors

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14
Q

quantal release

A

the release of neurotransmitters in a vesicle into the post synaptic cleft

large amt released per vesicle

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15
Q

quantal release triggers

A

either an IPSP or EPSP in the postsynaptic membrane

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16
Q

SNARE proteins

A

protines in the synaptic vesicle and presynaptic membrane that help dock the vesicles and zip together to force the membranes to fuse

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17
Q

what happens if SNARE proteins are destroyed/cleaved?

A

nuerotransmitters cannot be release from the synaptic vesicles

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18
Q

botulinum toxin

A

cleaves SNARE proteins preventing the release of NTs

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19
Q

where are small molecule NTs made?

A

terminal

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20
Q

where are peptides made?

A

cell body

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21
Q

Cholinergic

A

release Ach

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22
Q

Dopaminergic

A

release dopamine

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23
Q

noradrenergic

A

release norepiniphrine

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24
Q

glutamatergic

A

release glutamateG

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25
Q

GABAergic

A

release GABA

26
Q

peptidergic

A

release Peptide

27
Q

1 neuron can connect with _____other neurons

A

over 1000

axon terminals can synapse with any part of target neurons
- dendrite
- cell bodies
- axon

28
Q

motor unit

A

1 motor neuron and the muscle fibers it innervates

29
Q

neurons in the brains use

A

60% Glutamate
30% GABA

30
Q

NTs released by hypothalamus

A
  • thyrotropin-releasing hromone (TRH)
  • luteinizing hormone releaseing hormone (LHRH)
  • somatostatin
31
Q

NTs released by pituitary

A

-adrenocorticotropic hormone (ACTH)
-prolactin
-luteinising hormone
-thyrotropin
-growth hormone
-vasopressin
-oxytocin

32
Q

endorphine NTs

A

enkaphalins
opioids

33
Q

other NTs

A

substance P
bradykinin
angiotensin II

34
Q

Endocannabinoids (eCBs)
Mechanism

A
  • produced at postsynaptic neuron
  • flow back to presynaptic where it will bind to CB1 receptor, inhibiting Ca++
  • decrease NT release
35
Q

GABA w/out eCBs

A

GABA released from the presynaptic will inhibit postsynaptic NT release

decrease dopamine release (NT) release

***need to review slide 18

36
Q

GABA w/ eCBs

A

eCBs produced in postsynaptic neuron flow back to presynaptic CB1R

binding to CB1R inhibits Ca++ channels, decreasing GABA release.

Decreased GABA release will increase dopamine (NT) release

37
Q

Glutamate

A

Excitatory

Glutamate NT release from presynaptic will increase NT release from postsynaptic.

If eCBs present in postsynaptic, eCBs will bind to presynaptic CB1R, inhibiting Ca++ channels, decreasing Glutamate NT release. A decreased Glutamate release will decrease the postsynaptic NT release.

38
Q

Neurotransmitter receptor types

A
  1. ligan-gated ion channels
  2. g-protein coupled receptors
  3. enzyme linked receptors
39
Q

ligand-gated ion channels

A

ionotropic receptors
ion chanels

40
Q

G-protein coupled receptros

A

metabotropic receptors

41
Q

GABA Receptor

A

ligand-gated ion channel
GABA binds to receptor
ion channel opens
Cl- rushes into cell
hyperpolarization
(IPSP)

42
Q

agonist

A

chemical that activates a receptor to produce a biological response

43
Q

antagonist

A

A chemical substance that binds to and blocks the activation of certain receptors on cells, preventing a biological response.

44
Q

Isoflurane and GABA

A

isoflurane is a GABA agonist

facilitates ion channel opening and Cl- influx

45
Q

Propofol and GABA

A

propofol decreases the rate of dissociation of GABA from receptor

increase duration of GABA activated opening of Cl- channel

more Cl- influx
hyperpolarization (IPSP)

46
Q

ethanol and GABA

A

mimics GABAs effect on the braing by binding to GABA receptors and inhibiting neuronal signaling

IPSP and EPSP
IPSP: binding triggers Cl- influx

EPSP: mechanism unknown

47
Q

metabotropic receptors

A

activated G-protein diffuses in the membrane to act on its target, which may be an ion channel, enzymes, or gene transcription.

48
Q

Types of Ach receptors

A

ionotropic
metabotropic

49
Q

ionotropic Ach

A

nicotinic Ach receptor

skeletal muscle
brain
nerves

50
Q

metabotropic Ach

A

muscarinic Ach receptor

brain
peripheral organs

51
Q

ways to stop NT action

A
  1. reuptake
  2. breakdown
  3. diffusion
52
Q

reuptake

A

NTs can be returned to axon terminals for reuse or transported into glial cells

53
Q

breakdown

A

enzymes inactivate neurotransmitters

AchEsterase (AchE)

54
Q

diffusion (NT)

A

NTs can diffuse out of the synaptic cleft

55
Q

lidocaine

A

VG Na+ channel blocker

AP cannot be generated

56
Q

tetrodotoxin

A

VG Na+ channel blocker

depolarization inhibited

57
Q

botulinum toxin

A

cleaves SNARE proteins

decrease NT Ach release

58
Q

nerve gas

A

binds to AChE and disables AChE

increases ACh levels in synaptic cleft, triggers long lasting muscle contraction

59
Q

Curare

A

competitively bind to nAChR

less Ach can bind to receptor
less EpP generated
less AP generated
weakness in skeletal muscles

60
Q

MDMA

A

increases release of and binds to dopamine and 5-HT transporter

61
Q

Cocaine

A

binds to dopamine transporter

blocks dopamine uptake

increased dopamine in synaptic cleft

62
Q

SSRIs

A

bind to 5-HT transporter

blocks seratonin uptake

increased seratonin in synaptic cleft

Sp. Phys 1 (6 decks)

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