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A Synaptic Transmission > Tanner 1st third > Flashcards

Tanner 1st third Flashcards

1
Q

four CNS types

A

astrocytes
ependymal
microglial
oligodendrocytes

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2
Q

PNS types

A

satellite cells

schwann cells

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3
Q

ependymal cells

A 
line ventricles
produce CSF
form blood-CSF barrier
neural stem cells
precursors of neurons and astrocytes
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4
Q

myelin

A

lipid rich wrapping of glial membrane around axons to provide insulation and conduction

PNS: schwann cells
CNS: oligodendrocytes

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5
Q

PNS myelin

A

one schwann cell one axon

axons are sheathed by many schwanns

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6
Q

CNS myelin

A

one oligodendrocyte, multiple axons

axons may be sheathed by many oligodendrocytes

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7
Q

microglia

A 
smallest
star shaped
few processes
mesoderm derived (not ecto)
scavenger function/ macrophages
dormant
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8
Q

microglia respond to injury by

A 
mitosis
retract processes
product signal molecules
migrate to injury
destroy dying cells
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9
Q

astrocytes

A

many processes
end feet
ectoderm derived (neural origin)
CNS

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10
Q

astrocyte function

A

3D framework for CNS; guide neuronal migration along radial glia

repair damaged neural tissue

maintain BBB with end feet

metabolic support for neurons (break glucose down give lactate)

control ionic environment; aquaporins

uptake of NT

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11
Q

astrocyte synaptic functions

A

uptake GABA and Glu

express glutamate receptors, calcium entry alters shape

promote synapse formation w synaptogenic factors (tear down synapse, stabilize synapse)

envelop and isolate individual synapses

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12
Q

BBB

A

keeps out: pathogens, immune cells
allows to pass: O2,CO2,lipids passively; glucose, AA, hormones actively

compromise is bad

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13
Q

how do astrocytes bridge synaptic activity to blood flow??

A

neuronal activity locally incrases cerebral blood flow via vasodilation and increasing delivery of O2 and nutrients to neurons

glutamate reuptake by mGluR on astrocyte: signal for vasodilation

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14
Q

growth cone filopodia

A

test environment and attracted to some chemicals and repelled by others

signals transduced in cytoplasm of GC into motility and directional changes

depends on cyto calcium levels

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15
Q

axon guidance

A

elongation mediated by actin in filopodia and myosin

neurite MT backbone elongates w polymerization of tubulin and membrane is added to both sides via exocytosis

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16
Q

slit

A

dec cell motility

Ca - depoly - endocytosis - retraction

ROBO

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17
Q

netrin

A

inc motility

Ca - poly - exocytosis - elongation

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18
Q

intracellular Ca2+ regulates

A

Rho-GTPase effectors

protein pohsphatases (calcineurin)

protein kinases **poly, survival, not death, mitosis

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19
Q

types of cues

A

long range: soluble, secreted

short range: membrane bound, contact mediated

all act with gradient dependence

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20
Q

adhesion molecule interactions

A

CAM-CAM homophilic

Integrin-laminin heterophilic

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21
Q

axon crossing in spinal cord

A

first express netrin receptors and attract netrin in center

cross over; on robo receptor and repelled from midline

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22
Q

synapse formation

A

formation of selective contacts

differentiation of growth cone

elaboration of postsynaptic apparatus

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23
Q

synapse formation

A

axon guidance: cadherin and neuroligin

cell cell adhesion: homophilic with N-cadherins

synapse formation:heterophilic neurexin and neuroligin

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24
Q

cadherins

A

link to catenins; catenins link cyto domain of cadherins to actin cytoskeleton

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25
Q

NRX

A

neurexin interacts w presynaptic scaffold proteins

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26
Q

neuroligin NLG

A

post synaptic density scaffold proteins

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27
Q

what forms points for contact enabling recruitment of cytoplasmic scaffold proteins>

A

binding of neurexin to neuroligin

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28
Q

NMJ

A

large synapse
larger than average euk soma
nAChr

29
Q

patch clamping

A

suck hole draw it up

30
Q

activators

A 
acetylcholine
carbachol
nictoine
varenicline
glycopyrronium bromide
muscarine
31
Q

inhibitors

A

hexamethonium
tubocurarine
succinylcholine

32
Q

nAChr structure

A

2 binding sites, 5 subunits

bind on alpha

33
Q

electroplax

A

noncontracting muscle cells innervated by motor neuron
resting potential dominated by K+
nAChr on one side only

Ek = 90; ENa=60

5k rows in a series each with of 150mV

34
Q

nAChR desensitization

A

with time, closed desensitized slowly

35
Q

Reversal potential

A

point at which current charge switches

36
Q

Reversal potential stuff

A

PNa + PK = 1

PNa(60) + PK(-90) = 0

PNa = 0.6

37
Q

quantal hypothesis

A

NT is released from nerve terminals in discrete packets called quanta

38
Q

EPP

A

end plate potential postsynaptically

muscle EPSP

result of nAChR binding to NT; EPP followed by muscle AP

EPP drives AP

39
Q

mEPP

A

spontaneous, 1 vesicle

40
Q

evidence for QH

A

(m)EPP amp decreases with inc. distance from NMJ; mEPPs originate at NMJ synapse

mEPPs disappear upon motor axon removal; mEPPs arise from motor axon; EPPs from stimulation

(m) EPPs disappear upon application of ACh inhibitor; ACh NT action causes minis
(m) EPPs are mimicked by spritzing several thousand ACh to NMJ; mEPPs represent spontaneous release of discrete packets of ACh (quanta)

Stimulated EPPs have an mEPP shape and timecourse; synaptic potentials arise from simultaneous release of many quanta of NT

41
Q

Q

A

quantal size = amplitude of post synaptic response of ONE QUANTUM of NT ==== MINI

42
Q

M

A

quantal content/number

average number of presynaptic quanta released by one presynaptic AP

43
Q

vesicle hypothesis

A

axon terminals are filled w spherical vesicles

omega figures are evident in nerve terminal ms after electrical stimulation

vesicle depletion apparent after heavy stimulation

biochemical analysis has shown that vesicles are filled with NT

vesicles contain transporters that can be specific for the type of NT released from associated neuron

44
Q

vesicle hypothesis equation

A

c = dielectic constant*area / distance between surfaces

c = capacitance

C increases with AP because vesicle fusion increases SA

45
Q

vesicle fluoresence

A

fill vesicles w fluorescent NT - flash seen when vesicle fuses with membrane

46
Q

dense core vesicles

A

electron dense; peptide NT; more stimulation, further from active site

47
Q

stimulation (AP) only causes EPP in presence of

A

calcium to release NT

48
Q

one vesicle represents

A

1 quantum

49
Q

small clear core vesicles

A

small NT

active zone

lower stimulation

50
Q

why does TTX increase K0 and cause vesicular release

A

changing Ek for more positive

leak channels dominate

depolarization

ca2+ in

release

51
Q

excitation secretion

A

AP down axon

depolarization opens VGCCs

Ca2+ in

Ca2+ vinds synaptotagmin

detection of Ca triggers fusion and NT release

52
Q

postsynaptic current =

A

k[Ca2+]i^4

53
Q

SNARE Hypothesis

A

SNARE proteins on vesicle surface interact w snares on plasma membrane internal face

54
Q

vsnare

A

on vesicle

55
Q

SNAP

A

soluble NSF attachment protein

56
Q

NSF

A

n-ethykmaleimide sensitive factor

57
Q

Snare hypothesis experiment

A

N-ethylmaleimide binds in column

to purify NSF:

load sample, add NSF and it binds; wash

58
Q

use of purified NSF

A

sequence and use it to learn about SNAP

59
Q

use of purified SNAP

A

learn about it and learn snares

60
Q

Snare hypothesis stages of exocytosis

A

trafficking: movement of vesicles
tethering: restraint of vesicles
docking: binding of vesicles to membrane
priming: tight molecular interactions via SNARES
fusion: merging of membranes, release and inversion; ca2+ is signal REQUIRES ATP

61
Q

docking

A

SNAP25 and syntaxin on presynaptic plasma membrane

interacts with synaptobrevin on outside of vesicle membrane

62
Q

priming

A

SNARE complexes form to pull membranes together

ATP dependent

63
Q

Ca2+ sensing

A

entering Ca2+ binds to synaptotagmin

sensor: force trans to cis

rapid; 0.2ms – pore formation and vesicle fusion

64
Q

steps that are ATP dependent

A

priming

disengagement of SNARE complex

65
Q

after fusion

A

SNAPs bind NSF

bind SNARES and disengage

66
Q

endocytosis

A

translocation of fused membrane

clustering of vesicle proteins

clathrin coating - forms on intracellular side; guided by receptors

fission - invagination; pinching off from dynamin

recycling and refilling; decoating; merging of vesicle with endosome; retethering/filling

67
Q

buffers

A

control calcium and vesicular release

68
Q

what matters with calcium concentratioN?

A

distance and time

69
Q

facilitation

A

a temporary increase in synaptic strength

A Synaptic Transmission (2 decks)

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