Koide S, Onishi H, Katayama M, Yamagami S
Department of Neuropsychiatry, Osaka City University Medical School, Japan.
Neurochem Res. 1995 Mar;20(3):279-83. doi: 10.1007/BF00969543.
We previously suggested that a deficit of anticonvulsant endogenous methionine enkephalin, in the cerebral cortex, septal area, hippocampus, and striatum of seizure-susceptible El mice plays a role in the pathogenesis of seizures. To determine whether a hypofunction of enkephalinergic neuron may be due to metabolic abnormalities of opioid peptides in the El mouse brain, we measured methionine enkephalin-like immunoreactivity (ME-LI) of 50 fractions eluted by high performance liquid chromatography obtained from those four regions of the brain of El and seizure-nonsusceptible ddY mice (the mother strain of El mice). We observed the same ME-LI patterns of 50 fractions in the cerebral cortex and septal area in El and ddY mice, whereas exhibited differing ME-LI patterns in the hippocampus and striatum in the two stains. Different ME-LI patterns may imply the difference in the metabolic profile of opioid peptides. Thus, an abnormal metabolism of opioid peptides in the hippocampus and striatum of the El mouse may be involved in the pathogenesis of seizures.
我们之前曾提出,在易患癫痫的El小鼠的大脑皮层、隔区、海马体和纹状体中,抗惊厥内源性甲硫氨酸脑啡肽缺乏在癫痫发病机制中起作用。为了确定脑啡肽能神经元功能低下是否可能是由于El小鼠大脑中阿片肽的代谢异常所致,我们测量了从El小鼠和不易患癫痫的ddY小鼠(El小鼠的母系品系)大脑的这四个区域通过高效液相色谱洗脱得到的50个组分的甲硫氨酸脑啡肽样免疫反应性(ME-LI)。我们观察到El小鼠和ddY小鼠大脑皮层和隔区中50个组分的ME-LI模式相同,而在这两种品系的海马体和纹状体中ME-LI模式不同。不同的ME-LI模式可能意味着阿片肽代谢谱的差异。因此,El小鼠海马体和纹状体中阿片肽的异常代谢可能参与了癫痫的发病机制。