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幼龄和老龄大鼠新皮质中的神经肽Y和生长抑素:对基底核损伤的反应

Neuropeptide Y and somatostatin in the neocortex of young and aging rats: response to nucleus basalis lesions.

作者信息

Unger J W, Schmidt Y

机构信息

Department of Anatomy, University of Munich, Germany.

出版信息

J Chem Neuroanat. 1994 Jul;7(1-2):25-34. doi: 10.1016/0891-0618(94)90005-1.

DOI:10.1016/0891-0618(94)90005-1
PMID:7802968
Abstract

Lesions of the nucleus basalis of Meynert (NBM) have been used to mimic, in part, cholinergic deficits occurring in age-related neurodegenerative disorders, i.e., Alzheimer's disease. In our study, the effect of a persistent cholinergic denervation of the fronto-parietal cortex on neuropeptide Y (NPY) and somatostatin (SOM) was examined in young adult (3 months old) and aging (> 18 months old) rats, 1, 3 and 6 months after bilateral stereotaxic NBM lesions with quisqualic acid. In aging, non-lesioned rats a significant decrease in radioimmunologically and immunohistochemically detectable NPY and SOM was found with no further changes after lesions. Morphological markers for these peptidergic populations (cell size and number, NADPH-diaphorase histochemistry, electron microscopy) demonstrated no signs of alterations in both age groups after lesion. Densitometric analysis of peptide fibre networks displayed a heterogeneous response with a significant rarefication in young rats 1 month after the lesion, followed by restoration and a tendency towards increase 6 months post lesioning in individual animals. These findings were confirmed by radioimmunological measurements. Examination of synaptic and cytoskeletal markers, i.e., synaptophysin, GAP-43, MAP-2, Tau-1 and amyloid precursor protein, did not reveal any signs for neuronal reorganization or sprouting. These data are discussed in the context of plasticity and pathology in age-related neurodegenerative disorders with cholinergic impairment.

摘要

迈内特基底核(NBM)损伤已被用于部分模拟与年龄相关的神经退行性疾病(即阿尔茨海默病)中出现的胆碱能缺陷。在我们的研究中,在3个月大的年轻成年大鼠和超过18个月大的老龄大鼠中,用喹啉酸进行双侧立体定向NBM损伤后1、3和6个月,研究了额顶叶皮质持续性胆碱能去神经对神经肽Y(NPY)和生长抑素(SOM)的影响。在老龄未损伤大鼠中,放射免疫和免疫组织化学检测到的NPY和SOM显著减少,损伤后无进一步变化。这些肽能神经元群体的形态学标记(细胞大小和数量、NADPH-黄递酶组织化学、电子显微镜)显示,两个年龄组损伤后均无改变迹象。肽纤维网络的光密度分析显示出异质性反应,损伤后1个月年轻大鼠有显著稀疏,随后恢复,损伤后6个月个别动物有增加趋势。这些发现通过放射免疫测量得到证实。对突触和细胞骨架标记物(即突触素、GAP-43、MAP-2、Tau-1和淀粉样前体蛋白)的检查未发现神经元重组或发芽的任何迹象。在伴有胆碱能损伤的与年龄相关的神经退行性疾病的可塑性和病理学背景下讨论了这些数据。

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