Cuello A C, Maysinger D, Garofalo L
Department of Pharmacology and Therapeutics, McGill University, Montreal, Quebec, Canada.
Mol Neurobiol. 1992 Winter;6(4):451-61. doi: 10.1007/BF02757946.
The cholinergic pathway ascending from the nucleus basalis magnocellularis (NBM) to the cortex has been implicated in several important higher brain functions such as learning and memory. Following infarction of the frontoparietal cortical area in the rat, a retrograde atrophy of cholinergic cell bodies and fiber networks occurs in the basalocortical cholinergic system. We have observed that neuronal atrophy in the NBM induced by this lesion can be prevented by intracerebroventricular administration of exogenous nerve growth factor (NGF) or the monosialoganglioside GM1. In addition, these agents can upregulate levels of cortical choline acetyltransferase (ChAT) activity in the remaining cortex adjacent to the lesion site. Furthermore, an enhancement in cortical high-affinity 3H-choline uptake and a sustained in vivo release of cortical acetylcholine (ACh) after K+ stimulation are also observed after the application of neurotrophic agents. Moreover, these biochemical changes in the cortex are accompanied by an anatomical remodeling of cortical ChAT-immunoreactive fibers and their synaptic boutons.
从基底前脑大细胞基底核（NBM）上行至皮质的胆碱能通路与学习和记忆等多种重要的高级脑功能有关。大鼠额顶叶皮质区域梗死之后，基底皮质胆碱能系统中胆碱能细胞体和纤维网络会发生逆行性萎缩。我们观察到，通过脑室内给予外源性神经生长因子（NGF）或单唾液酸神经节苷脂GM1，可以预防这种损伤诱导的NBM神经元萎缩。此外，这些药物可以上调损伤部位相邻的剩余皮质中皮质胆碱乙酰转移酶（ChAT）的活性水平。此外，应用神经营养药物后，还观察到皮质高亲和力3H-胆碱摄取增加以及K+刺激后皮质乙酰胆碱（ACh）在体内的持续释放。此外，皮质中的这些生化变化伴随着皮质ChAT免疫反应性纤维及其突触小体的解剖重塑。
