Opioid-induced epileptogenic phenomena: anatomical, behavioral, and electroencephalographic features.
Recent animal studies have indicated a possible role of opioids in epilepsy. Intraventricular opioid administration induces a prolonged nonconvulsive stuporous state characterized by epileptiform electroencephalographic patterns, and reversed by naloxone. In high doses, naloxone itself causes generalized clonic convulsions. We compared opioid-induced and naloxone-induced epileptogenic phenomena using quantitative 2-deoxyglucose autoradiography in order to define the anatomical structures involved in these two different seizure types. When opioid-induced seizures occurred, limbic structures were preferentially activated, but when naloxone-induced clonic convulsions occurred, pyramidal and extrapyramidal motor areas and some limbic structures were activated. Based on the present experiments and currently available evidence, we speculate that opioid-mediated epileptogenic phenomena are similar to those occurring during the postictal state of a fully kindled seizure, whereas naloxone-induced epileptogenic phenomena are similar to the ictal state. Therefore, simple pharmacological manipulation of endogenous opioid systems may allow selective study of ictal and postictal phenomena.
D000818:Animals; D001345:Autoradiography; D001522:Behavior, Animal / Q000187:drug effects*; D003847:Deoxyglucose; D004569:Electroencephalography; D004744:Enkephalin, Methionine / Q000494:pharmacology*; D004827:Epilepsy / Q000139:chemically induced* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D009270:Naloxone / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains
D009270:Naloxone; D004744:Enkephalin, Methionine; D003847:Deoxyglucose