Mechanism of action of Antiepileptic Drugs

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Presentation transcript:

Mechanism of action of Antiepileptic Drugs B. Gitanjali Gitanjali-1:

Cellular Mechanisms of Seizure Generation Excitation (too much) • Ionic-inward Na+, Ca++ currents • Neurotransmitter: glutamate, aspartate Inhibition (too little) • Ionic-inward Cl; outward K+ currents • Neurotransmitter: GABA Gitanjali-5:

AEDs: Molecular and Cellular Mechanisms Phenytoin, Carbamazepine • Block voltage-dependent sodium channels at high firing frequencies Gitanjali-6:

Na+ Open Activation gate Na+ Inactivation gate Na+ Gitanjali-7:

Block channels firing at high frequencies Na+ Block channels firing at high frequencies Inactivated channel Na+ Na+ Na+ Carbamazepine Phenytoin Felbamate Lamotrigine Barbiturates Topiramate Gitanjali-8:

AEDs: Molecular and Cellular Mechanisms Barbiturates • Prolong GABA-mediated chloride channel openings • Some blockade of voltage- dependent sodium channels Gitanjali-9:

AEDs: Molecular and Cellular Mechanisms Benzodiazepines • Increase frequency of GABA- mediated chloride channel openings Gitanjali-10:

AEDs: Molecular and Cellular Mechanisms Valproate May enhance GABA transmission in specific circuits Blocks voltage-dependent sodium channels Blocks T-type calcium currents Gitanjali-11:

Cl- Gabapentin Vigabatrin Valproate Gabapentin Benzodiazepines GT Succinic Semialdehyde Valproate SSD metabolites Gabapentin Tiagabine Benzodiazepines Barbiturates Topiramate Cl- GT: GABA transaminase SSD:Succinic semialdehyde dehydrogenase Gitanjali-12:

AEDs: Molecular and Cellular Mechanisms Ethosuximide •Blocks slow, threshold, “transient” (T-type) calcium channels in thalamic neurons Gitanjali-13:

Voltage regulated Ca++ current, low threshold “T” current in thalamus Involved in 3 per second spike and wave rhythm Ca++ Gitanjali-14:

Ca++ Ethosuximide Valproate Reduction in the flow of Ca++ through T - type Ca++ channels in thalamus Gitanjali-15:

Newer AEDs: Molecular and cellular Mechanisms Vigabatrin • Irreversibly inhibits GABA- transaminase Tiagabine • Interferes with GABA re-uptake Gitanjali-16:

Newer AEDs: Molecular and cellular Mechanisms Topiramate Blocks voltage-dependent sodium channels at high firing frequencies Increases frequency at which GABA opens Cl- channels (different site from benzodiazepines) Antagonizes glutamate actions at receptor subtype Gitanjali-17:

Newer AEDs: Molecular and Cellular Mechanisms Felbamate • May block voltage-dependent sodium channel at high firing frequencies • May modulate NMDA receptor via strychnine insensitive glycine receptor Gitanjali-18:

AEDs: Molecular and Cellular Mechanisms Gabapentin • May modulate amino acid transport into brain • May interfere with GABA re-uptake Gitanjali-19:

Newer AEDs: Molecular and Cellular Mechanisms Lamotrigine • Blocks voltage-dependent sodium channels at high firing frequencies • May interfere with pathologic glutamate release Gitanjali-20: