Limbic postictal events: anatomical substrates and opioid receptor involvement.
1. Amygdaloid kindled seizures in rats produce postictal motor deficits, disruption of affective responding to sensory input, postictal explosiveness, and seizure suppression that may be similar to events following complex partial seizures in humans. 2. Preliminary 2DG studies in kindled rats indicate that postictal motor deficits may be mediated by the substantia nigra. Disruption of affective responding and postictal seizure suppression may be mediated by the hippocampus. 3. Data from the literature indicates that postictal motor deficits may be mediated by mu and kappa opioid receptors. The disruption of affective responding may be mediated primarily be delta and maybe also by kappa receptors. Postictal explosiveness may involve either a non-mu receptor or it may be a non-opioid effect. Kindling-induced postictal seizure suppression may be mediated by kappa receptors and perhaps also by mu receptors. 4. Mechanisms underlying postictal effects of complex partial seizures in humans are suggested by the data in this manuscript. New approaches to the treatment of these postictal events are also proposed.
Caldecott-Hazard
S
S
Department of Neurology, Reed Neurological Institute, Los Angeles, California.
Engel
J
J
D000818:Animals; D003847:Deoxyglucose / Q000378:metabolism; D004195:Disease Models, Animal; D004723:Endorphins / Q000502:physiology*; D004833:Epilepsy, Temporal Lobe / Q000503:physiopathology*; D008032:Limbic System / Q000503:physiopathology*; D009043:Motor Activity / Q000187:drug effects; D009270:Naloxone / Q000494:pharmacology; D051381:Rats; D011957:Receptors, Opioid / Q000502:physiology
D004723:Endorphins; D011957:Receptors, Opioid; D009270:Naloxone; D003847:Deoxyglucose