Dua A K, Pinsky C, LaBella F S
Electroencephalogr Clin Neurophysiol. 1985 Dec;61(6):569-72. doi: 10.1016/0013-4694(85)90976-9.
In 3 different models of opioid epileptogenesis we have utilized opioid receptor antagonists to differentiate the nature and role of opioid receptor subtypes involved in opioid agonist-induced epileptoid responses in rats. Selective mu-opioid receptor agonism can initiate epileptoid responses in non-dependent rats. Delta-opioid agonism is important in sustaining mu-initiated epileptoid responses. A role for mu-opioid receptor stimulation in delta-opioid initiated epileptoid responses remains yet to be clarified. Delta-opioid antagonism does not precipitate classic autonomic and behavioral signs of withdrawal in morphine-dependent rats but blocks epileptoid responses in naloxone-precipitated morphine withdrawal without affecting autonomic and behavioral components of an ongoing withdrawal reaction.
在3种不同的阿片类药物致癫痫模型中，我们使用阿片受体拮抗剂来区分参与阿片类激动剂诱导大鼠癫痫样反应的阿片受体亚型的性质和作用。选择性μ-阿片受体激动可在非依赖性大鼠中引发癫痫样反应。δ-阿片激动在维持μ-引发的癫痫样反应中很重要。μ-阿片受体刺激在δ-阿片引发的癫痫样反应中的作用仍有待阐明。δ-阿片拮抗作用不会在吗啡依赖大鼠中引发经典的自主神经和戒断行为体征，但可阻断纳洛酮诱发的吗啡戒断中的癫痫样反应，而不影响正在进行的戒断反应的自主神经和行为成分。
