GABA synapse and epilepsy Flashcards
Describe the sequence of events at the GABA synapse
Na influx - depolarisation
GABA in vesicles - 40-100000 molecules in each vesicle
vesicles primed so form a close association with the membrane
synaptotagmin in calcium channels
calcium ion channel near primed vesicles - can get rapid response to local calcium influx
drive fusion of vesicles and exocytosis
GABA in synapse
some binds to GABA receptors - other molecules don’t but if enough bind many Cl- may enter
chloride channel opens - 35000 move in through each channel every 1.5ms
at glial cell: GABA transporter - GABA – succinate semialdehyde by GABA transaminase, carbon skeleton is recycled
in nerve cell GABA transporter replenishes vesicles
use of epilepsy drug
wide use
can be used in combination of other drugs
and with different types of epilepsy
for specific types of epilepsy you can use specific drugs
why don’t drugs modulate the glutamate synapse
don’t want to block the receptors because there are many functions
action of tiagabine
inhibits GABA entering the GABA-T and so GABA stays in synapse for longer - have more of an effect
action of vigabatrin
inhibit GABA transaminase
so increases level of GABA
action phenobarbital
bind to GABA receptor
potentiate response - channel is open longer
action of diazepam
bind to GABA receptor
potentiate response
increase the frequency of opening