1 / 17

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)

mindy
Download Presentation

Mechanism of action of Antiepileptic Drugs

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  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:

More Related