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Excitatory glutamatergic and synaptic plasticity - Coggle Diagram
Excitatory glutamatergic and synaptic plasticity
ionotrophic receptor
tetramer (4 part)
AMPA + NMDA
AMPA activates first because Mg temp blocks NMDA
Na influx
unblocks Mg
NMDA prolongs depolarisation
NMDA
made up of GluN subunit
1
2A-D
3A/B
is blocked by Mg by -60mV
needs
glutamate
and
glycine/D-serine
to fully activate
N1 binds to glycine/D-serine
N2 binds to glutamate
N residue is the Mg site
AMPA
Glu
A1-3
heteromers
needs GluA2 because it impairs Ca permeability and prevent polyamine block (the rest are susceptible to these)
Ca permeability is due to the R within the pore instead of Q
this difference is due to RNA editing/
adenosine deamination
which is adenosine -> inosine
spermine
blocks all AMPA except A2
trafficking and density
transported in vesicles (by microtubules)
exocytosis from the dendrites
movement is stabilised by scaffold proteins
internalised near the synapse by endocytosis
Kainate
GluK
1-5
model of subunit
ATD
amino terminal domaiN
CTD
carboxy terminal domain
M1-4
transmembrane domain
S1-2
ligand binding domain
synaptic plasticity/
long term potentiation
high freq stimulation relieves Mg block on NMDA
increase of Ca allows translocation of
CaMKII
and phosphorylation of AMPAR subunits
seems to be related to A1/2 interaction with various C terminus
research needed for Huntington
disease
EPSP integration
the summation of enough post synaptic excitation to get an action potential
temporal summation
: multiple action potentials in succession
spatial summation
: multiple synaptic inputs simultaneously