Anti-seizure meds

Question 1

Mechanism Carbamazepine

Answer 1

-stabilizes “inactivated” state of VG Na+ channels –> decrease in repetitive firing
Presynaptic –> diminish glutamate release

Question 2

Mechanism ethosuximide

Answer 2

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

Question 3

Levetiracetam mechanism

Answer 3

Affects synaptic vesicle protein SV2A, resulting in decreased glutamate release but increased GABA release
Synaptic vesicle proteins in presynaptic neurons

Question 4

Topiramate mech

Answer 4

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)

Question 5

Phenytoin mech

Answer 5

Prolongs Inactivation phase of v-gated sodium channels which prevents rapid firing of action potentials; also see decreased glutamate release (presynaptic)

Question 6

valproic acid mech

Answer 6

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

Question 7

phenobarbital mech

Answer 7

GABA-A: Increase in the duration of chloride channel-opening events; Also depress the excitatory actions glutamate via binding to the AMPA receptor

Question 8

Diazepam/lorazepam mech

Answer 8

GABA-A: Increase in the frequency of chloride channel-opening events

Question 9

Gabapentin

Answer 9

Designed as GABA analog, but primarily inhibits high-voltage-activated Ca2+ channels (decreases Ca2+ entry)