title: Modification of effects of chronic electroconvulsive shock by voltage-dependent Ca2+ channel blockade with nifedipine.
abstract: A single electroconvulsive shock produced analgesia (expressed as prolongation of hot-plate latency) in Wistar rats 45 min after the shock. The analgesic action was prevented by administration of nifedipine, 5 mg/kg i.p., 15 min before the electroconvulsive shock, while nifedipine injection after electroconvulsive shock did not affect the analgesia significantly. At the same time single electroconvulsive shock counteracted the reduction of [3H]nitrendipine binding to cortical and hippocampal membranes from rats pretreated with nifedipine. Chronic administration of electroconvulsive shock (once daily for 8 days) produced hyperalgesia, augmented locomotor responses to low doses of apomorphine and upregulation of cortical (but not hippocampal) voltage-dependent Ca2+ channels (assessed from [3H]nitrendipine binding). In rats receiving electroconvulsive shock chronically, always 15 min after nifedipine injection, neither behavioral hyperresponsiveness nor Ca2+ channel upregulation was observed. The results suggest that the primary event in post-electroconvulsive shock analgesia depends on Ca2+ influx into neurons through voltage-dependent Ca2+ channels, and that given under conditions of Ca2+ channel blockade electroconvulsive shock is unable to trigger changes leading to Ca2+ channel upregulation, and this is possibly the reason for prevention of development of hyperalgesia and increased responsiveness to dopaminergic stimulation.
authors.affiliation: Department of Biochemistry, Polish Academy of Sciences, Krakow.
authors.forename: L
authors.initials: L
authors.lastname: Antkiewicz-Michaluk
authors.forename: J
authors.initials: J
authors.lastname: Michaluk
authors.forename: J
authors.initials: J
authors.lastname: Vetulani
mesh_terms: D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D001522:Behavior, Animal / Q000187:drug effects; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism; D004597:Electroshock; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism; D006930:Hyperalgesia / Q000503:physiopathology; D008297:Male; D008566:Membranes / Q000187:drug effects / Q000378:metabolism; D009043:Motor Activity / Q000187:drug effects; D009543:Nifedipine / Q000494:pharmacology*; D009568:Nitrendipine / Q000493:pharmacokinetics; D051381:Rats; D017208:Rats, Wistar; D012640:Seizures / Q000503:physiopathology*; D015854:Up-Regulation / Q000187:drug effects; D015430:Weight Gain / Q000187:drug effects
chemical_list: D002121:Calcium Channel Blockers; D015220:Calcium Channels; D009568:Nitrendipine; D009543:Nifedipine; D001058:Apomorphine