epliepsy Flashcards
the recurrent seizures are due to
abnormal neuronal excitability
uncontrolled glutamate excitability in cns
why may happen in many forms of epilepsy
GABA transmition not working properly
GABA synthesised by
decarboxylation of glutamate
what enzymes
glutamic acid decarboxylase (GAD)
what happens once GABA is exocytosed into synapse
. GABA reversibly binds post-synaptic receptors (linked to ion channels
what does that cause
opening of chloride ion channels, allowing chloride influx into post synaptic terminal
causes to the PSNT
hyperpolarises the PSNT
futher away from resting potential
harder to reach an AP
how is it inactivated in the PreSNT
- Rapid uptake of GABA by GABA transporters (GATs)
how is it inactivated by glial cells
. GABA enzymatically modified by GABA-transaminase (GABA-T) to succinic semialdehyde (glial cells & GABA nerve terminals)
structure of GABA A receptor
and why its important
Pentameric organisation of the GABA receptor provides pharmacologically important binding domains
what is epilepsy
the over excitation in a particular area of the brain
what is type drug is diazepam
positive allosteric modulator not an agonist
mediates/facilatates GABA binding to receptor
so when does it have no effect
has NO effect in the absence of GABA
what does Lamotrigine target
Voltage gated sodium channel
it inhibits the release of which NT
glutamate
