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NEURO 0010 > Lectures 4-5 : Synapse > Flashcards

Lectures 4-5 : Synapse Flashcards

1
Q

where does an electrical synapse occur?

A

gap junction

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2
Q

what proteins form a gap junction channel? what are they made of?

A
  • 2 connexons
  • 6 connexins for a connexon
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3
Q

what flows through a gap junction?

A

materials such as small molecules, or ions

there is a current that passes equally well on both sides

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4
Q

what does an AP become in a gap junction?

A

PSP - postsynaptic potential

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5
Q

what is unique about gap junction synapses?

A

they are bi directional

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6
Q

where are gap junctions most commonly located? what are the cells that form gap junctions called?

A

glial cells or areas where synchronization is important

electrically coupled

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7
Q

how could a PSP trigger an action potential?

A

PSPs are small about 1mV, therefore several PSPs are needed to strongly excite a cell

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8
Q

where does a chemical synapse occur?

A

the synaptic cleft

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9
Q

what are membrane differentiations?

A

dense accumulation of proteins on wither side of the synaptic cleft

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10
Q

what are the types of membrane differentiations?

A
  • active zones
  • postsynaptic density
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11
Q

what is the active zone?

A

area on presynaptic cell at which neurotransmitter is released

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12
Q

what is the post synaptic density?

A

contains receptors which turn the chemical signal to electrical signals

NT –> AP

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13
Q

what is the synaptic vesicle?

A

membrane delineated vesicles that contain NT

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14
Q

signal conversation pathway?

A
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15
Q

types of synapses axons can have?

A
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16
Q

what is a specialized synapse?

A

neuromuscular junction

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17
Q

what occurs at a neuromuscular junction synapse?

A

neuron terminates on motor end-plate of muscle fiber - very reliable and fast transmission

they are large

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18
Q

acronym for NT release pathway?

A

S - synthesis
R - release
A - action
T - termination

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19
Q

what happens to vesicles when NT are released?

A

vesicles fuse with membrane and release contents into the cleft

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20
Q

what are the two types of vesicles? what do they store?

A

clear = small molecules
dark = large molecules

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21
Q

what is dales principle?

A

for neurotransmitter synthesis pathways, neuron only contains the enzymes necessary to synthesize that neurotransmitter but none of the subsequent enzymes needed to convert it into later products

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22
Q

what is the exception to dales prinicple?

A

many peptide-containing neurons can release a neurotransmitter along with a peptide

co transmitters
- can release 2 or more neurotransmitters simontaneaously

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23
Q

what are the 3 types of NT? what are the NTs they produce?

A

1) Amino acids
- GABA, Glycine
2) Amines
- monoamines: serotonin/5- HT, acetylcholine
- Catecholines: dopamine - norepinephrine
epinephrine
3) Peptides

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24
Q

how does the release of a peptide differ?

A
  • cells needs to be stimulates more – it takes more Ca to
    trigger the release
  • Ca channels are much closer to vesicles
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25
Q

what did otto loewi’s experiment do?

A

confirmed the existence of chemical (NTs)

both frog hearts slowed, when gate was opened

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26
Q

what is vagussstoff?

A

ACh

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27
Q

vSNARES vs tSNARES

A

vSNARES = proteins in the vesicle involved in docking
tSNARES = on the presynaptic membrane (terminal axon), helps anchor vesicle.

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28
Q

what is synaptotagmin?

A

protein found in SNARE complex, Ca2+
sensing protein

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29
Q

what do NT when they are released from synapse?

A

bind to receptors on the other side

cause depolarization or hyperpolarization

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30
Q

what ions move when the cell hyper-polarizes? depolarizes?

A
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31
Q

what are the kinetics of how fast a change in the charge of a membrane occurs?

A
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32
Q

overall NT release pathway?

A

1) action potential travels down the axon
2) arrives at terminal button
3) terminal button depolarizes
4) Vesicles fuse with membrane, release contents into
synaptic cleft

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33
Q

what does the speed and direction of a change in charge depend on?

A

Ion

Type of receptor`

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34
Q

What are the 3 known NT receptor types?

A

Ligand- gated
Auto recpetors
G- protein couples receptors

35
Q

what is an EPSP?

A

depolarization of the postsynaptic membrane potential by the action of a synaptically released neurotransmitter

36
Q

what are ways of generating ESPS?

A

increasing Na+ conductance

37
Q

what are NTs that are excitatory?

A

glutamate

38
Q

what is an IPSP?

A

a change in the postsynaptic membrane potential by the action of a synaptically released neurotransmitter, making the postsynaptic neuron less likely to fire action potentials.

39
Q

what NTs are inhibitory?

A

GABA and glycine

40
Q

what is a method of generating IPSPs?

A

increasing Cl- conductance

41
Q

what are the neuropharmacology of receptors

A

antagonists
- binds to receptor and inhibits NT from binding

receptor agonist
- binds to the receptors, mimics its normal activity

inhibitor
- inhibits the normal function of specific proteins involved in synaptic transmission

42
Q

what are agonist examples?

A
  • nicotine
43
Q

what is a ligand?

A

the NT that binds to a receptor

44
Q

what are the parts of a ligand gated receptor? what are they made of–how can they differ?

A

subunits that go through the membrane

single polypeptide chain
subunits have different amino acid subunits that come together to make different subtypes

45
Q

what are examples of the subunits and subtypes of receptor?

A

Glutamate
- AMPA (Na, K+)
- NMDA (Na, K, Ca)
- kainate (Na, K)

46
Q

ligand gated channel pathway?

A
47
Q

selectivity : ligand vs. VG channels?

A

ligand is less selective

48
Q

speed : ligand vs. G-protein?

A

ligand are faster but G-proteins have longer

49
Q

what are autoreceptors?

A

on presynaptic cell

activated by the NT they release

generally are GPCRs which then go on to regulate some aspect of the cell

50
Q

phosphorylation definition and agent?

A
  • adds phosphate group to protein
  • carried out by protein kinase
51
Q

dephosphorilization

A
  • remove phosphate from protein
  • carried out by protein phosphatase
52
Q

what are g proteins made of? specifics?

A

a single polypeptide chain that passes through the membrane 7 times

53
Q

what are G protein effetcs like?

A

slower, stronger, longer lasting, with more diverse effects on the postsynaptic cell

54
Q

what are the subunits of a gprotein?

A

alpha
gamma
beta

55
Q

ionotropic receptors 3 facts and example?

A
56
Q

metabotropic receptors?

A
57
Q

what are two receptors that bind ACh?

A
58
Q

components of g- protein activation?

A

Neurotransmitter
Receptor
G- protein
Alpha, gamma & beta subunits
Effector protein
GDP & GTP

59
Q

components of cAMP signaling?

A

Receptor – GPCR
G- protein – Gs
Effector enzyme – Adenylyl cyclase (AC)
Substrate of effector enzyme – ATP
Second messenger – cAMP
Protein kinase – Protein kinase A (cAMP dependent protein kinase)

60
Q

components of Phosphoinositide or DAG?

A

What are the components?
Receptor – GPCR
G-protein – Gq
Effector enzyme – PLC
Substrate of effector enzyme – PIP2
Second messengers
- DAG
- IP3
- CA2+
Intermediaries
- IP3-R
- ER
- CaM
Protein kinases
- PKC
- Ca/CaM kinase

61
Q

what ions correlate with glutamate, ACh, GABA and glycine?

A
62
Q

excitatory vs. inhibitory?

A

EPSP - IPSP

63
Q

stimulatory vs. inhibitory

A

excite post synaptic - inhibit post synaptic

64
Q

how much energy does a little packet of neurotransmitter have? what are these small energies called?

A

about .5mV - miniature endplate potentials

65
Q

what is synaptic intergration?

A

the process by which multiple synaptic potentials combine in one post synaptic neuron

66
Q

what is quantal analysis?

A

the smallest unit of neurotransmission is the release of the contents in one vesicle
- mini
- all ESPs are multiple of the mini

67
Q

how can synaptic integration happen?

A

spatial summation
temporal summation

68
Q

what is spatial summation?

A

adding together of many ESPS generated at the same time on multiple synapses of a dendrite

69
Q

what is temporal summation?

A

adding together of ESPs that occur close together in time

70
Q

what is the length constant?

A

quantifies the length that depolarization travels before decaying to 37% of its original strength

  • further away from the spike trigger zone on the axon, the less likely it is that an AP will be generated
  • longer the length constant = neuron is better at preventing dissipation of depolarization
  • longer the length constant = more likley that EPSP at a distant synapse will cause an AP
71
Q

what are the kinds of dendrites?

A

passive
excitable

72
Q

how do passive dendrites function?

A
  • depolarization decreases along axon, loosing charge
73
Q

how do excitable dendrites function?

A
  • voltage gated sodium channels are on the dendrite, depolarization spreads and opens channels
  • lets in more depolarization
  • depolarization spreads
  • oscillations of Vm due to activation of voltage gated ion channels
74
Q

how do G proteins increase length constant?

A
  • protein kinases can function by either opening of closing channels
75
Q

internal resistance & membrane resistant concerning :
def, what resistance depends on, results when inc, results when dec

A
76
Q

shunting Inhibition

A

when an inhibitory synapse is activated close to the soma, the resultant IPSP can work to cancel out the incoming EPSP

this is called shunting inhibition because this inhibitory synapse near the soma can “shunt” away excitation and prevent the neuron from firing

the neuron is held at a membrane potential below threshold

77
Q

what are the ways that a signal can be terminated?

A

diffusion
re uptake
degradation

78
Q

desensitization

A

continued exposure to high concentration of NT makes channels stop responding

79
Q

diffusion process?

A

neurotransmitter simply diffuses out of the synaptic cleft down its concentration gradient

e. NO - nitric oxide

80
Q

re uptake process?

A

NT is retrieved from the synaptic cleft for processing and re-use –> can be degraded by enzymes or transported into vesicles

Ex. 5-HT reuptake transporters

81
Q

degradation process?

A

enzymatic inactivation of the NT

Ex. acetylcholinesterase destroys ACh

82
Q

Removal of specific NT’s (ACh, Catecholines, serotonin, amino acids)

A
83
Q

Termination of events in Postsynaptic Cell

A

NEURO 0010 (22 decks)

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