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一种神经生长因子肽可延缓癫痫大鼠模型中癫痫发作的发展并抑制神经元发芽。

A nerve growth factor peptide retards seizure development and inhibits neuronal sprouting in a rat model of epilepsy.

作者信息

Rashid K, Van der Zee C E, Ross G M, Chapman C A, Stanisz J, Riopelle R J, Racine R J, Fahnestock M

机构信息

Department of Biomedical Sciences, McMaster University, Hamilton, ON Canada.

出版信息

Proc Natl Acad Sci U S A. 1995 Oct 10;92(21):9495-9. doi: 10.1073/pnas.92.21.9495.

Abstract

Kindling, an animal model of epilepsy wherein seizures are induced by subcortical electrical stimulation, results in the upregulation of neurotrophin mRNA and protein in the adult rat forebrain and causes mossy fiber sprouting in the hippocampus. Intraventricular infusion of a synthetic peptide mimic of a nerve growth factor domain that interferes with the binding of neurotrophins to their receptors resulted in significant retardation of kindling and inhibition of mossy fiber sprouting. These findings suggest a critical role for neurotrophins in both kindling and kindling-induced synaptic reorganization.

摘要

点燃效应是一种癫痫动物模型,通过皮层下电刺激诱发癫痫发作,可导致成年大鼠前脑神经营养因子mRNA和蛋白质上调,并引起海马苔藓纤维发芽。脑室内注入一种模拟神经生长因子结构域的合成肽,该肽可干扰神经营养因子与其受体的结合,导致点燃效应显著延迟,并抑制苔藓纤维发芽。这些发现表明神经营养因子在点燃效应和点燃效应诱导的突触重组中都起着关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3dc/40828/81bfe9189cae/pnas01499-0079-a.jpg

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