β-内啡肽可诱发非惊厥性边缘叶癫痫发作。
beta-Endorphin induces nonconvulsive limbic seizures.
作者信息
Henriksen S J, Bloom F E, McCoy F, Ling N, Guillemin R
出版信息
Proc Natl Acad Sci U S A. 1978 Oct;75(10):5221-5. doi: 10.1073/pnas.75.10.5221.
Abstract
The endogenous opioid peptide, beta-endorphin, induces nonconvulsive limbic epileptiform activity when administered intraventricularly to rats. Epileptiform activity is elicited by beta-endorphin in doses that are devoid of analgesic or behavioral signs. Equimolar intraventricular doses of morphine or of the enkephalin analog [DAIa2,Met5]enkephalin-NH2 fail to elicit this limbic epileptiform activity. These observations, together with the recent immunohistochemical localization of beta-endorphin to midline limbic structures, suggest that beta-endorphin may have an important role in the regulation of limbic excitability.
摘要
内源性阿片肽β-内啡肽经脑室注射给大鼠时，会诱发非惊厥性边缘叶癫痫样活动。β-内啡肽在不产生镇痛或行为体征的剂量下就能引发癫痫样活动。等摩尔剂量的吗啡或脑啡肽类似物[DAIa2,Met5]脑啡肽-NH2经脑室注射未能引发这种边缘叶癫痫样活动。这些观察结果，连同最近β-内啡肽在中线边缘叶结构的免疫组织化学定位，提示β-内啡肽可能在边缘叶兴奋性调节中起重要作用。
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