Anti-seizure meds Flashcards
Mechanism Carbamazepine
-stabilizes “inactivated” state of VG Na+ channels –> decrease in repetitive firing
Presynaptic –> diminish glutamate release
Mechanism ethosuximide
Blocks VG T-type dependent Ca channel, disrupting pacemaker activity; Works on thalamic neurons, which may stop them from generating rhythmic cortical discharges that occur during absence seizures
Presynaptic
Levetiracetam mechanism
Affects synaptic vesicle protein SV2A, resulting in decreased glutamate release but increased GABA release
Synaptic vesicle proteins in presynaptic neurons
Topiramate mech
Increased inactivation of VG Na+ channels
- blocks presynaptic (N; P/Q) VG Ca2+ channels
- enhances GABAa-receptor currents (not via BZD receptor)
- limits activation of AMPA-kainate subtypes of the glutamate receptor (post synaptic)
Phenytoin mech
Prolongs Inactivation phase of v-gated sodium channels which prevents rapid firing of action potentials; also see decreased glutamate release (presynaptic)
valproic acid mech
Decreases repetitive firing, potentially via multiple mechanisms: block of VG Na+, NMDA receptor block, decreases GABA reuptake (GAT-1); reduces the flow of Ca2+ through T-type Ca2+ channels
phenobarbital mech
GABA-A: Increase in the duration of chloride channel-opening events; Also depress the excitatory actions glutamate via binding to the AMPA receptor
Diazepam/lorazepam mech
GABA-A: Increase in the frequency of chloride channel-opening events
Gabapentin
Designed as GABA analog, but primarily inhibits high-voltage-activated Ca2+ channels (decreases Ca2+ entry)