Rocha L, Engel J, Ackermann R F
Department of Neurology, UCLA 90024.
Epilepsy Res. 1991 Nov-Dec;10(2-3):103-10. doi: 10.1016/0920-1211(91)90002-w.
Effects of chronic naloxone pretreatment (75 or 270 micrograms/h for 14 days) on the development of amygdaloid kindling in rats were evaluated. The acquisition of seizure activity was modified in the naloxone pretreated animals, depending on the nucleus stimulated: facilitation of stages IV and V occurred in 37%, variability of electrographic and behavioral responses to electrical stimulation during the kindling development in 33%, and facilitation of stages IV and V followed by long periods of seizure suppression in 29%. Enhancement of postictal seizure suppression during a recycling paradigm was observed in all the naloxone pretreated rats. It was concluded that the chronic administration of naloxone (known to induce opioid binding upregulation and supersensitivity), in association with the enduring changes in opioid mechanisms provoked by kindled seizures, were responsible for the facilitation and suppression of epileptic activity. These findings support bidirectional modulatory effects of opioid peptides on epileptic seizures as well as the view that epileptic seizures can induce enduring alterations in opioid mechanisms.
评估了慢性纳洛酮预处理(75或270微克/小时,持续14天)对大鼠杏仁核点燃发展的影响。在纳洛酮预处理的动物中,癫痫活动的获得发生了改变,这取决于所刺激的核团:37%的动物出现IV期和V期的促进,33%的动物在点燃发展过程中对电刺激的脑电图和行为反应出现变异性,29%的动物出现IV期和V期的促进,随后是长时间的癫痫抑制。在所有纳洛酮预处理的大鼠中,在循环范式期间观察到发作后癫痫抑制增强。得出的结论是,纳洛酮的慢性给药(已知会诱导阿片类物质结合上调和超敏反应),与点燃性癫痫发作引起的阿片类机制的持久变化相关,是癫痫活动促进和抑制的原因。这些发现支持阿片肽对癫痫发作的双向调节作用,以及癫痫发作可诱导阿片类机制持久改变的观点。