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Mechanism of action of Antiepileptic Drugs

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)

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Mechanism of action of Antiepileptic Drugs

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

  2. 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:

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

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

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

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

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

  8. 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:

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

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

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

  12. Ca++ Ethosuximide Valproate Ca++ Reduction in the flow of Ca++ throughT - type Ca++ channels in thalamus Gitanjali-15:

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

  14. 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:

  15. 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:

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

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

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