Antiabsence drugs and inhibitory pathways.
Conditioning stimuli to the coronal gyrus or periventricular gray matter inhibit the activity of spinal trigeminal neurons. Valproate decreased the corticofugal inhibition of the spinal trigeminal nucleus, as did ethosuximide, trimethadione, and imipramine. Valproate and ethosuximide also decreased the periventricular inhibition of the spinal trigeminal nucleus, indicating that antiabsence drug depress subcortical inhibitory pathways as well as pathways of cortical origin. These results support the hypothesis that ability to depress inhibitory pathways is an important characteristic of antiabsence drugs. The effect of valproate and ethosuximide on periventricular inhibition also suggests that these anticonvulsants may act by preventing the spread of seizure activity through subcortical pathways.
D000818:Animals; D000927:Anticonvulsants / Q000494:pharmacology* / Q000627:therapeutic use; D002415:Cats; D002552:Cerebral Ventricles / Q000187:drug effects; D004832:Epilepsy, Absence / Q000188:drug therapy* / Q000503:physiopathology; D005013:Ethosuximide / Q000627:therapeutic use; D007099:Imipramine / Q000627:therapeutic use; D009433:Neural Inhibition / Q000187:drug effects*; D009434:Neural Pathways / Q000187:drug effects*; D014293:Trimethadione / Q000627:therapeutic use; D014635:Valproic Acid / Q000627:therapeutic use
D000927:Anticonvulsants; D005013:Ethosuximide; D014635:Valproic Acid; D007099:Imipramine; D014293:Trimethadione