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biomembranes > excitatory transmission > Flashcards

excitatory transmission Flashcards

1
Q

what are the 3 main types of ionotropic glutamate receptors defined by

A

the actions of the selective agonists AMPA, kainate and NMDA

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2
Q

when a cell is at -60mV, what is the net flow of inward current mainly carried by

A

Na+ and Ca2+ ions entering the cell

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3
Q

how are ionotropic glutamate receptor channels activated

A

selectively

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4
Q

what is magnesimum

A

a voltage- and use-dependant blocker of the NMDA receptor associated ion channel

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5
Q

what does the NMDAR conduct when activated

A

Na+, Ca2+ and K+

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6
Q

how does the NMDAR channel open

A

it needs to be activated by glutamate or NMDA and by the co-agonist glycine

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7
Q

what are blockers of the NMDAR ion channel

A

phencyclidine (PCP) and ketamine

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8
Q

what do ketamine and PCP act as

A

clinically as an anaesthetic

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9
Q

how is magnesium unblocked

A

through depolarising the cell

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10
Q

what happens at +20mV

A

the net flow of current is outward - mainly by K+ ions leaving the cell
Mg2+ does not enter or block the cell

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11
Q

what effect does Mg2+ have at -60mV

A

they block NMDA-evoked single channel openings in a concentration-dependant manner

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12
Q

what effect does Mg2+ have at +40mV

A

no effect

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13
Q

where does glutamate bind

A

GluN2 subunit

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14
Q

where does glycine bind

A

GluN1 subunit

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15
Q

what happens in the absence of glycine

A

glutamate does induce a current (due to activation of AMPARs)

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16
Q

what happens in the presence of glycine

A

the current is greatly increase as now glutamate additionally activates NMDARs

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17
Q

what is APV

A

a NMDAR selective receptor antagonist

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18
Q

what is CNQX

A

an AMPAR antagonist

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19
Q

explain the synergistic interplay of synaptic AMPAR and NMDAR at an excitatory synapse

A

neurally released glutamate activates the synaptic AMPARs, but although glutamate also bind to NMDARs the associated ion channel does not initially conduct due to ion channel blockage from MG2+ which happens almost immediately
the Na+ influx caused by activation of AMAPR causes a depolarisation of the neuronal spine. if the presynaptic glutamatergic nerve fires at high frequenciesm or multiple glutamatergic inputs are stimulated then the depolarisation may be sufficient to cause MG2+ unblocking of the NMDA receptor and consequently the appearance of a slow prolonged synaptic depolarisation, mediated by NMDARs
high frequencies of presynaptic activity will favour NMDAR activation

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20
Q

what facilitates NMDAR activation

A

high frequencies of presynaptic activation and stimulation of multiple glutamatergic input neurons

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21
Q

what is EPSP

A

excitatory postsynaptic potential

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22
Q

what increases postsynaptic depolarisation

A

repeptitive stimulation, or the stimulation of multiple glutamatergic inputs

23
Q

what is the structure of all ionotropic glutamate receptors

A

tetrameric assemblies of 4 subunits

24
Q

what are the subunits of NMDA

A

GluN1, GluN2A,B,C,D, GluN3A,B

25
Q

what are the subunits of AMPA

A

GluA1,2,3,4

26
Q

what are the subunits of kainate

A

GluK1,2,3,4,5

27
Q

what is the structural difference between ionotropic glutamate receptor subunits and ionotropic cys-loop receptor subunits

A

1 =tetramer - AMPA receptor - GluA1-4
2 = pentamer - nicotinic receptors, 5HT3 receptors, GABAa receptors, glycine receptors

28
Q

what are the majority of AMPARs

A

heteromers containing the GluA2 subunit

29
Q

what are AMPARs composed of

A

GluA1, 3 or 4 subunits

30
Q

what are AMPARs permeable to

A

Ca2+

31
Q

what are AMPARs blocked by

A

endogenous polyamines

32
Q

which subunit of AMPARs is critical in determining receptor function

A

GluA2

33
Q

what does incorporation of GluA2 subunits to AMPARs do

A

impairs Ca2+ permeability and prevents polyamine block

34
Q

what is the permeability of Ca2+ in AMPARs dictated by

A

the nature of a single AA located in the ion conducting pore
glutamine Q = permeable
arginine R = impermeable

35
Q

what is the GluA2 subject to, and what does this detemined

A

RNA editing
whether the GluA2 subunit contains a Q or R residue at the ion channel

36
Q

in the adult, how much of the GluA2 is edited

A

95%

37
Q

what regulates calcium permeability

A

M2 Q/R-site

38
Q

what does spermine do

A

acts as an intracellular AMPAR ion channel antagonist to block the outward current carried by cations. it only blocks the GluA2-subunit lacking AMPARs and the non-edited GluA2 AMPARs

39
Q

what is an ionotropic glutamate receptor subunit composed of

A

ATD (amino terminal domain)
CTD (caboxy terminal domain)
M1-4 (transmembrane domains)
S1-2 (ligand-binding domain)

40
Q

what are the majority of NMDARs composed of

A

GluN1 and GluN2 subunits

41
Q

what do NMDAR subunits have a similar topology to

A

the AMPA and kainate subunits

42
Q

what does the GluN1 subunit bind

A

glycine

43
Q

what does the GluN2 subunit bind

A

glutamate

44
Q

on the NMDARs, what is the asparagine residue (N) responsible for

A

site of Mg2+ block

45
Q

what are quantum dots (QD)

A

tiny semiconductor particles (nanometer)

46
Q

how are the movement of receptors in live neruones monitored

A

Using fluorescent quantum dots & high resolution microscopy

47
Q

what must be present for efficient synaptic transmission

A

postsynaptic receptors must cluster opposite presynaptic release sites

48
Q

what is the number of synaptic receptors dictated by

A

the interplay of reversible receptor stabilization &​ a dynamic equilibrium between pools of receptors in synaptic, extrasynaptic & intracellular compartments.​

49
Q

describe the AMPA receptor trafficking in and out of the postsynaptic density

A

Newly synthesized receptors are transported intracellularly in vesicles by molecular motors on microtubules. ​
Vesicle exocytosis in the dendritic shaft.
Once at the cell surface, receptors move randomly.
The receptors are reversibly stabilized by diffusion trapping at the post-synaptic density (PSD) through interactions with intracellular & extracellular scaffold proteins.
Diffusing receptors internalized at extrasynaptic endocytic zones by clathrin-dependent endocytosis.
Endocytosed receptors can be recycled back by exocytosis.

50
Q

what is the expression and location of AMPARs influenced by

A

neuronal activity – a basis for synaptic plasticity e.g. LTP.
exposure to acute & chronic stress.
neurodegenerative disorders e.g. Alzheimer’s Disease, Huntington’s disease.
by various drugs – e.g. ketamine, cocaine.

51
Q

what does LTP stand for

A

long term potentiation

52
Q

what is LTP induced by

A

a burst of high frequency stimulation (HFS)

53
Q

explain the process of AMPAR trafficking and LTP

A

1) High-frequency stimulation relieves the magnesium block of the NMDAR to increase intracellular calcium allowing within seconds translocation of CaMKII (pink) to spines​ & subsequent phosphorylation of the γ2 and γ8 AMPAR auxiliary subunits.​
2) This leads to increased binding of AMPARs to PSD95 resulting in their accumulation​ at the Post Synaptic Density (PSD) through diffusion-trapping. ​
3) In parallel, intracellular AMPARs, either newly synthesized, or from recycling compartments, are exocytosed within minutes of the stimulation, largely in the dendritic shaft, but also in the ​spine.​
4) These AMPARs are delivered to the cell surface then replenish the extrasynaptic pool & further diffuse to the synapse.​

54
Q

how does stabilising of AMPARs in the synapse occur

A

via an interaction of the C terminus ​with various interactor proteins & these interactors differ for GluA1 & GluA2.

biomembranes (9 decks)

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