肽诱导的婴儿癫痫持续状态会导致神经元死亡和突触重组。
Peptide-induced infant status epilepticus causes neuronal death and synaptic reorganization.
作者信息
Baram T Z, Ribak C E
机构信息
Childrens Hospital Los Angeles, Department of Neurology, University of Southern California 90027, USA.
出版信息
Neuroreport. 1995 Jan 26;6(2):277-80. doi: 10.1097/00001756-199501000-00013.
Abstract
Status epilepticus (SE) produced by excitatory amino acids is a well established model in adult rodents. Limbic neuronal degeneration and synaptic reorganization observed after, for example, kainic acid-induced SE are considered relevant to human epilepsy. Kainic acid also produces severe seizures in infant rats, but neuronal injury and sprouting have not been demonstrated. The results of the present study show that corticotropin releasing hormone (CRH)-induced SE causes limbic neuronal death and reorganization in infant rats. In adults, CRH produced seizures at much higher doses, and no neuronal degeneration. As a modulator of the CNS stress response, CRH is activated in various 'stressful' circumstances. Its age-dependent ability to kill neurons represents a unique form of cell death potentially important in human medicine.
摘要
由兴奋性氨基酸引起的癫痫持续状态（SE）在成年啮齿动物中是一个成熟的模型。例如，在海藻酸诱导的SE后观察到的边缘神经元变性和突触重组被认为与人类癫痫有关。海藻酸在幼鼠中也会引发严重癫痫发作，但尚未证实有神经元损伤和发芽现象。本研究结果表明，促肾上腺皮质激素释放激素（CRH）诱导的SE会导致幼鼠边缘神经元死亡和重组。在成年动物中，CRH在高得多的剂量下才会引发癫痫发作，且没有神经元变性。作为中枢神经系统应激反应的调节剂，CRH在各种“应激”情况下被激活。其随年龄变化的杀死神经元的能力代表了一种在人类医学中可能具有重要意义的独特细胞死亡形式。
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