Gasser U E, Weskamp G, Otten U, Dravid A R
Brain Res. 1986 Jun 25;376(2):351-6. doi: 10.1016/0006-8993(86)90198-8.
Axotomy of cholinergic neurons in the medial septum-diagonal band and degeneration of their terminals in the hippocampus resulting from fornix-fimbria lesions induce elevation of NGF content in these two brain regions. Postlesion levels of cholinergic neuron-specific ChAT activity in the septum suggest that endogenously produced NGF may, at least partly, promote survival of axotomized cholinergic neurons or induce ChAT activity in undamaged cells or both. These findings thus support the proposed trophic role for NGF in central cholinergic neurons.
穹窿-海马伞损伤导致内侧隔核-斜角带胆碱能神经元轴突切断及其海马终末变性，可引起这两个脑区神经生长因子（NGF）含量升高。损伤后隔核中胆碱能神经元特异性胆碱乙酰转移酶（ChAT）活性水平表明，内源性产生的NGF可能至少部分促进轴突切断的胆碱能神经元存活，或诱导未受损细胞中的ChAT活性，或两者皆有。因此，这些发现支持了NGF在中枢胆碱能神经元中所提出的营养作用。
