GALANINERGIC INNERVATION OF THE CHOLINERGIC VERTICAL LIMB OF THE DIAGONAL BAND (CH2) AND BED NUCLEUS OF THE STRIA TERMINALIS IN AGING, ALZHEIMER-DISEASE AND DOWN-SYNDROME
GALANINERGIC INNERVATION OF THE CHOLINERGIC VERTICAL LIMB OF THE DIAGONAL BAND (CH2) AND BED NUCLEUS OF THE STRIA TERMINALIS IN AGING, ALZHEIMER-DISEASE AND DOWN-SYNDROME
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DOI：
10.1159/000107329
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发表时间：
1993-09-01
期刊：
影响因子：
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通讯作者：
KORDOWER, JH
中科院分区：
文献类型：
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作者：
MUFSON, EJ;COCHRAN, E;KORDOWER, JH
含有甘丙肽（GAL）的肽纤维系统回路支配含有乙酰胆碱的基底前脑神经元，其已被证明在阿尔茨海默病（AD）中肥大并过度支配剩余的胆碱能Ch 4胞体。本研究探讨是否发生类似的hypernervedition内的胆碱能垂直肢体的斜角带核（Ch 2），基底前脑的一部分，不像Ch 4，只表现出适度的退化，在AD。此外，我们评估了GAL神经支配是否发生在唐氏综合征的基底前脑内，唐氏综合征是一种遗传性疾病，具有广泛的AD样病理，包括胆碱能基底前脑神经元变性。本研究表明，几乎所有的Ch 2神经元GAL免疫阴性。然而，这一地区的支配GAL免疫反应（IR）的中间神经元和纤维与一个主要的甘丙肽能途径，通过无名质的路线，下丘脑，床核的终纹以及垂直分支的斜角带核。与年龄匹配的对照组和唐氏病例相比，AD患者在该纤维束内的GAL-免疫反应纤维肥大。在AD的推定的Ch 2终末区，尽管Ch 2神经元适度减少，但许多剩余的胆碱能神经元被GAL过度支配。与此相反，GAL-IR纤维并没有肥大的唐氏综合征，尽管广泛的胆碱能细胞损失Ch 4。总之，这些研究结果表明，广泛的胆碱能基底前脑细胞损失单独是不足以触发基底前脑GAL可塑性反应中发现的AD。
The galanin (GAL) containing peptide fiber system circuit which innervates acetylcholine containing basal forebrain neurons has been shown to hypertrophy and hyperinnervate remaining cholinergic Ch4 perikarya in Alzheimer's disease (AD). The present study examined whether a similar hyperinnervation occurs within the cholinergic vertical limb of the diagonal band nucleus (Ch2), a portion of the basal forebrain which, unlike Ch4, exhibits only modest degeneration in AD. Furthermore, we evaluated whether GAL hyperinnervation occurs within the basal forebrain in Down's syndrome, a genetic disorder with extensive AD-like pathology including cholinergic basal forebrain neuron degeneration. The present study revealed that virtually all Ch2 neurons were GAL immunonegative. However, this region was innervated by GAL immunoreactive (ir) interneurons and fibers associated with a major galaninergic pathway which travels through the substantia innominata enroute to the hypothalamus, bed nucleus of the stria terminalis as well as vertical limb of diagonal band nucleus. GAL-ir fibers coursing within this fiber bundle hypertrophied in AD relative to age matched controls and the Down's cases. Within the putative Ch2 terminal zones in AD, many of the remaining cholinergic neurons were hyperinnervated by GAL despite the modest reduction in Ch2 neurons. In contrast, GAL-ir fibers were not hypertrophied in Down's syndrome despite extensive cholinergic cell loss within Ch4. Taken together these findings suggest that extensive cholinergic basal forebrain cell loss alone is not sufficient to trigger the basal forebrain GAL plasticity response found in AD.