Parvalbumin-immunoreactive neurons and GABAergic neurons of the basal forebrain project to the rat basolateral amygdala.
Parvalbumin-immunoreactive neurons and GABAergic neurons of the basal forebrain project to the rat basolateral amygdala.
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DOI：
10.1016/j.neuroscience.2009.02.077
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发表时间：
2009-06-02
期刊：
影响因子：
3.3
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中科院分区：
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基底前脑（BF）包含一个弥散排列的胆碱能和非胆碱能神经元，这些神经元投射到大脑皮层和杏仁核基底外侧核复合体（BLC）。以前的研究表明，GABA能亚群的非胆碱能皮质BF神经元选择性地支配皮质中间神经元。尽管在啮齿类动物和灵长类动物中的一些研究表明，一些投射到BLC的BF神经元是非胆碱能的，但还没有研究试图鉴定这些神经元的神经化学表型。本研究结合荧光金逆行追踪和免疫组织化学的两个标记的BF GABA能神经元，小清蛋白（PV）或谷氨酸脱羧酶（GAD），以确定是否有一个亚群的BF GABA能细胞的项目，以BLC。荧光金注射局限于大鼠BLC，并集中在基底外侧核，产生广泛的逆行标记腹侧苍白球和无名质的BF地区。虽然绝大多数的逆行标记的神经元没有双重标记，约10%的这些神经元，主要位于沿着腹侧方面的纹状体和苍白球，表现出PV或GAD的免疫反应。这项研究的结果与长期以来的信念相矛盾，即BLC没有GABA能输入的杏仁核外来源，并表明皮质样BLC除了皮质本身外，还接受来自基底前脑的抑制性输入。
The basal forebrain (BF) contains a diffuse array of cholinergic and non-cholinergic neurons that project to the cerebral cortex and basolateral nuclear complex of the amygdala (BLC). Previous studies have shown that the GABAergic subpopulation of non-cholinergic corticopetal BF neurons selectively innervates cortical interneurons. Although several investigations in both rodents and primates have indicated that some BF neurons projecting to the BLC are non-cholinergic, there have been no studies that have attempted to identify the neurochemical phenotype(s) of these neurons. The present study combined Fluorogold retrograde tract tracing with immunohistochemistry for two markers of BF GABAergic neurons, parvalbumin (PV) or glutamic acid decarboxylase (GAD), to determine if a subpopulation of BF GABAergic cells projects to the BLC. Injections of Fluorogold confined to the rat BLC, and centered in the basolateral nucleus, produced extensive retrograde labeling in the ventral pallidum and substantia innominata regions of the BF. Although the great majority of retrogradely labeled neurons were not double-labeled, about 10% of these neurons, located mainly along the ventral aspects of the fundus striati and globus pallidus, exhibited immunoreactivity for PV or GAD. The results of this investigation contradict the long-held belief that there is no extra-amygdalar source of GABAergic inputs to the BLC, and indicate that the cortex-like BLC, in addition to the cortex proper, receives inhibitory inputs from the basal forebrain.