Unger J W, Schmidt Y
Department of Anatomy, University of Munich, München, FRG.
Neurosci Lett. 1993 Apr 30;153(2):140-3. doi: 10.1016/0304-3940(93)90307-7.
The neuropeptide Galanin (Gal) is known to play a functional role in the basal forebrain cholinergic system. In our study, the morphology and density of the Gal-immunoreactive (Gal-IR) fiber network within the cholinergic nucleus basalis of Meynert (NBM) was investigated 1, 3 and 6 months after stereotaxic lesion with quisqualic acid in young adult (3 months old) and late middle-aged (20 months old) rats. Quantitative densitometry showed a significantly reduced Gal-IR fiber network in 20-month-old control rats. After lesion-induced cholinergic cell loss, no further changes in Gal-IR were noted in this group of aging rats during the period of investigation. In contrast, young adult animals displayed a significant increase of Gal-IR fiber density 6 months after NBM lesion. However, no hyperinnervation of individual surviving cholinergic neurons was seen. The results obtained in an animal model of cholinergic deficit support the hypothesis of age-related neuroplasticity of specific transmitter and peptide systems. Adaptive changes in Gal may play a role for the modulation of cholinergic function and could be of importance in human age-related neurodegenerative disorders, i.e. Alzheimer's disease.
已知神经肽甘丙肽（Gal）在前脑基底胆碱能系统中发挥功能作用。在我们的研究中，对年轻成年（3个月大）和中老年（20个月大）大鼠在立体定位注射quisqualic酸损伤后1个月、3个月和6个月时，Meynert基底核（NBM）胆碱能核内甘丙肽免疫反应性（Gal-IR）纤维网络的形态和密度进行了研究。定量密度测定显示，20个月大的对照大鼠中Gal-IR纤维网络显著减少。在损伤诱导胆碱能细胞丢失后，在该组老龄大鼠的研究期间未观察到Gal-IR的进一步变化。相比之下，年轻成年动物在NBM损伤6个月后Gal-IR纤维密度显著增加。然而，未观察到单个存活胆碱能神经元的超神经支配。在胆碱能缺陷动物模型中获得的结果支持了特定递质和肽系统与年龄相关的神经可塑性假说。Gal的适应性变化可能在胆碱能功能的调节中起作用，并且在人类与年龄相关的神经退行性疾病（即阿尔茨海默病）中可能具有重要意义。
