Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neuroscience > Postsynaptic > Flashcards

Postsynaptic Flashcards

1
Q

entry of sodium in post synaptic neuron causes

A

depolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

structure of a dendritic spine

A

small membranous protrusion from a neuron dendrite that typically receives input from a single axon at the synapse
dendritic spine = spine neck + spine head
storage sites for synaptic strength and help transmit electrical signals to the neuons cell body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

why are dendritic spines important

A

functional compartmentalisation
ionic and biochemical changes are partially restricted to just the activated synapse - input specificity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

post synaptic density

A

neurotransmitter receptors and anchored and regulated by a host protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

where do eneurons receive inputs

A

somato dendritic compartments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how is L Glutamate synthesised

A
  • non essential amino acid
  • synthesised from glutamine via glutaminase
  • most abundant excitatory neurotransmitter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

injected intracerebral glutamate results in

A

seizures
shown by Hayashi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

where is glutamate stored

A

synaptic vesicles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how is glutamate transported into vesicles

A

VGLUT transfers cytosolic glutamate into vesicle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how is glutamate released

A

calcium dependent release mechanism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

glutamate receptors

A

specific protein targets
iGluRs
mGluRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

where are glutamate transporters present

A

pre and post synaptic nerve terminals and astrocytes (EAAT1/2)
rapid removal of transmitter from synapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

process for glutamate synthesis

A

glutamate-glutamine shuttle and metabolic processes within presynaptic terminal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

2 main types of ionotropic receptors

A

AMPA
NMDA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

AMPA receptor role

A

day to day business of synaptic communication
they are permeable to sodium and potassium ions but do not usually pass calcium ions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

NMDA receptor role

A

activated under special conditions
pass calcium ions as well as sodium and potassium
this calcium flux allows local biochemical changes to be triggered when the receptors are activated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

structure of a single iGluR subunit

A

extracellular = N terminus and ligand binding domain
Intracellular = C terminus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Glu subunits in AMPA

A

mixtures of gutA1-4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

why do most AMPA receptors contain GluA2

A

endows calcium impermeabile to the pore

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

example antagonists of AMPA receptors

A

NBQX
CNQX

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Glu subunits in NMDA receptors

A

mixtures of GluN1 and GluN2 - must have both

22
Q

calcium and NMDA receptors

A

calcium permeable pore
voltage dependent magnesium block

23
Q

example antagonist of NMDA receptors

A

AP5

24
Q

are NMDA and AMPA tetrameric and heterotetramers

A

NMDA and AMPA = tetrameric assemblies
NMDA = always heterotetramers
AMPA = usually heterotetramets

25
Q

what is fast synaptic transmission mediated by

A

ionotropic receptors

26
Q

EPSP of AMPA receipts

A

high amplitude short lived EPSP

27
Q

when is the magnesium block on NMDA channel removed

A

at a voltage of - 35nV (depolarising potentials
= magnesium block is removed

28
Q

NMDA receptor EPSP

A

NMDA receptor mediated a slow rising long lasting EPSP = via sodium and calcium entry through channel

29
Q

one inside the cell what can calcium cause

A

calcium can activate enzymes
regulate ion channel opening and affect gene expression
result in changes to synaptic strength -> synaptic plasticity

30
Q

GABA full name and role

A

gamma-amino butyric acid
major inhibitory neurotransmitter in the brain

31
Q

what are the2 classes of GABA receptor

A

GABA (a) - ionotropic - fast
GABA (b) - metabotropic - slow

32
Q

how is GABA synthesised from glutamate

A

Glutamte + glutamate decarboxylase = GABA

33
Q

where is GABA stored

A

synaptic vesicles

34
Q

how is GABA transported to vesicle

A

transporter VGAT transfers cytosolic GABA into vesicle

35
Q

how is GABA vesicle

A

calcium dependent release

36
Q

where are GAT1 and GAT3 transporters present

A

pre and post synaptic nerve terminals
process for rapid removal of transmitters from synapse GABA transporters

37
Q

what are the 2 isodorms of glutamate decarboxylase (GAD)

A

GAD67 - through cell
GAD65 - nerve terminal

37
Q

what are the 2 isodorms of glutamate decarboxylase (GAD)

A

GAD67 - through cell
GAD65 - nerve terminal

38
Q

wants the key difference between location of GABAergic and glutamergic synapses

A

GABAergic synapses do not usually occur on dendritic spines

39
Q

structure of GABA(a) receptors

A

pentameric ligand acted chloride channels
4 transmembrane domains
5 subunits - 2xalpha, 2xbeta, gamma

40
Q

what transmembrane protein forms the pore of GABA channel

A

TM2

41
Q

what ion causes hyperpolasiation through GABA receptors

A

chloride ions - flow down EC gradient into the cell = hyperpolarise the cell

42
Q

what receipts are most widely used for synaptic inhibition

A

GABA(a)

43
Q

what happens when GABA binds to GAbA a receptors

A

cholride ions flow inside
produce fat inhibitor postsynaptic potential (IPSP)

44
Q

what type of receptor are GABAG (b)

A

heterodimeric GPCR - metabotropic receptor
slower

45
Q

how do GABA (b) receptors work

A

GPCR
inhibits voltage gated calcium channel
modulate the activity of adenylyl cyclase and amount of cAMP = suppress downstream effects
slower IPSP

46
Q

where are GABA b receptors commonly found

A

pre synaptic terminals

47
Q

why does activation of GABA b receptors produce sloe IPSP

A

works via second messengers - slower

48
Q

what does co activation of GABA a and GABA b produce

A

long lasting biphasic IPSPs

49
Q

what is an autoreceptor

A

receptor on presynaptic terminal - activated by the neurotransmitter released by the synapse

50
Q

what can the presence of GABAb auto receptors lead to

A

form of paired pulse depression
2 identical presynaptic stimuli are given in rapid succession - second IPSP is smaller

51
Q

why do GABA b auto receptors lead to paired pulse depression

A
  • activation of presynaptic GABAb receptors is negatively coupled to voltage gated calcium channels
  • restricts Ca2+ entry to presynaptic cell
  • conditioned (2nd) stimuli results in reduced Ca2+-dependent exocytosis –> less GABA released

Neuroscience (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions