Postsynaptic Flashcards
entry of sodium in post synaptic neuron causes
depolarisation
structure of a dendritic spine
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
why are dendritic spines important
functional compartmentalisation
ionic and biochemical changes are partially restricted to just the activated synapse - input specificity
post synaptic density
neurotransmitter receptors and anchored and regulated by a host protein
where do eneurons receive inputs
somato dendritic compartments
how is L Glutamate synthesised
- non essential amino acid
- synthesised from glutamine via glutaminase
- most abundant excitatory neurotransmitter
injected intracerebral glutamate results in
seizures
shown by Hayashi
where is glutamate stored
synaptic vesicles
how is glutamate transported into vesicles
VGLUT transfers cytosolic glutamate into vesicle
how is glutamate released
calcium dependent release mechanism
glutamate receptors
specific protein targets
iGluRs
mGluRs
where are glutamate transporters present
pre and post synaptic nerve terminals and astrocytes (EAAT1/2)
rapid removal of transmitter from synapse
process for glutamate synthesis
glutamate-glutamine shuttle and metabolic processes within presynaptic terminal
2 main types of ionotropic receptors
AMPA
NMDA
AMPA receptor role
day to day business of synaptic communication
they are permeable to sodium and potassium ions but do not usually pass calcium ions
NMDA receptor role
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
structure of a single iGluR subunit
extracellular = N terminus and ligand binding domain
Intracellular = C terminus
Glu subunits in AMPA
mixtures of gutA1-4
why do most AMPA receptors contain GluA2
endows calcium impermeabile to the pore
example antagonists of AMPA receptors
NBQX
CNQX
Glu subunits in NMDA receptors
mixtures of GluN1 and GluN2 - must have both
calcium and NMDA receptors
calcium permeable pore
voltage dependent magnesium block
example antagonist of NMDA receptors
AP5
are NMDA and AMPA tetrameric and heterotetramers
NMDA and AMPA = tetrameric assemblies
NMDA = always heterotetramers
AMPA = usually heterotetramets
what is fast synaptic transmission mediated by
ionotropic receptors
EPSP of AMPA receipts
high amplitude short lived EPSP
when is the magnesium block on NMDA channel removed
at a voltage of - 35nV (depolarising potentials
= magnesium block is removed
NMDA receptor EPSP
NMDA receptor mediated a slow rising long lasting EPSP = via sodium and calcium entry through channel
one inside the cell what can calcium cause
calcium can activate enzymes
regulate ion channel opening and affect gene expression
result in changes to synaptic strength -> synaptic plasticity
GABA full name and role
gamma-amino butyric acid
major inhibitory neurotransmitter in the brain
what are the2 classes of GABA receptor
GABA (a) - ionotropic - fast
GABA (b) - metabotropic - slow
how is GABA synthesised from glutamate
Glutamte + glutamate decarboxylase = GABA
where is GABA stored
synaptic vesicles
how is GABA transported to vesicle
transporter VGAT transfers cytosolic GABA into vesicle
how is GABA vesicle
calcium dependent release
where are GAT1 and GAT3 transporters present
pre and post synaptic nerve terminals
process for rapid removal of transmitters from synapse GABA transporters
what are the 2 isodorms of glutamate decarboxylase (GAD)
GAD67 - through cell
GAD65 - nerve terminal
what are the 2 isodorms of glutamate decarboxylase (GAD)
GAD67 - through cell
GAD65 - nerve terminal
wants the key difference between location of GABAergic and glutamergic synapses
GABAergic synapses do not usually occur on dendritic spines
structure of GABA(a) receptors
pentameric ligand acted chloride channels
4 transmembrane domains
5 subunits - 2xalpha, 2xbeta, gamma
what transmembrane protein forms the pore of GABA channel
TM2
what ion causes hyperpolasiation through GABA receptors
chloride ions - flow down EC gradient into the cell = hyperpolarise the cell
what receipts are most widely used for synaptic inhibition
GABA(a)
what happens when GABA binds to GAbA a receptors
cholride ions flow inside
produce fat inhibitor postsynaptic potential (IPSP)
what type of receptor are GABAG (b)
heterodimeric GPCR - metabotropic receptor
slower
how do GABA (b) receptors work
GPCR
inhibits voltage gated calcium channel
modulate the activity of adenylyl cyclase and amount of cAMP = suppress downstream effects
slower IPSP
where are GABA b receptors commonly found
pre synaptic terminals
why does activation of GABA b receptors produce sloe IPSP
works via second messengers - slower
what does co activation of GABA a and GABA b produce
long lasting biphasic IPSPs
what is an autoreceptor
receptor on presynaptic terminal - activated by the neurotransmitter released by the synapse
what can the presence of GABAb auto receptors lead to
form of paired pulse depression
2 identical presynaptic stimuli are given in rapid succession - second IPSP is smaller
why do GABA b auto receptors lead to paired pulse depression
- 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
