Dekker A J, Fagan A M, Gage F H, Thal L J
Department of Neurosciences, University of California, San Diego.
Brain Res. 1994 Mar 7;639(1):149-55. doi: 10.1016/0006-8993(94)91775-2.
Rats received a unilateral lesion of the nucleus basalis magnocellularis (NBM) by infusion of ibotenic acid. Starting 2 weeks after the lesion, the animals were treated with nerve growth factor (NGF) or brain-derived neurotrophic factor (BDNF) by intraparenchymal infusion of 3 micrograms per day for 4 weeks. Lesioned control animals received a similar amount of cytochrome c. The activity of choline acetyltransferase (ChAT) in the frontal neocortex was significantly reduced by the lesion (-39%). However, the intraparenchymal treatment with NGF or BDNF did not affect cortical ChAT activity. The number of p75 NGF receptor-immunoreactive neurons in the NBM was significantly decreased (-49%) by the lesion and was not affected by NGF or BDNF. The size of the remaining neurons was significantly increased by NGF (+32%), but not by BDNF (+12%). Similarly, in situ hybridization showed enhanced expression of the p75 NGF receptor following treatment with NGF, but not with BDNF. These results suggest that although BDNF occurs in the target area of cholinergic NBM neurons, its effects on these neurons are less pronounced than those of NGF.
通过注入鹅膏蕈氨酸,使大鼠的基底大细胞核(NBM)受到单侧损伤。损伤后2周开始,通过脑实质内每天注入3微克的神经生长因子(NGF)或脑源性神经营养因子(BDNF),持续4周。损伤对照组动物接受等量的细胞色素c。额叶新皮质中胆碱乙酰转移酶(ChAT)的活性因损伤而显著降低(-39%)。然而,脑实质内给予NGF或BDNF并不影响皮质ChAT活性。损伤使NBM中p75 NGF受体免疫反应性神经元的数量显著减少(-49%),且不受NGF或BDNF的影响。NGF使剩余神经元的大小显著增加(+32%),但BDNF未使其增加(+12%)。同样,原位杂交显示,用NGF治疗后p75 NGF受体的表达增强,但BDNF治疗后未增强。这些结果表明,尽管BDNF存在于胆碱能NBM神经元的靶区域,但其对这些神经元的作用不如NGF明显。