2-MERCAPTOACETATE AND 2-DEOXY-D-GLUCOSE INDUCE FOS-LIKE IMMUNOREACTIVITY IN RAT-BRAIN
2-MERCAPTOACETATE AND 2-DEOXY-D-GLUCOSE INDUCE FOS-LIKE IMMUNOREACTIVITY IN RAT-BRAIN
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DOI：
10.1016/0006-8993(94)91822-8
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发表时间：
1994-03-28
期刊：
影响因子：
2.9
通讯作者：
DINH, TT
中科院分区：
文献类型：
--
作者：
RITTER, S;DINH, TT
2-脱氧-D-葡萄糖（2-DG）和2-巯基乙酸（MA）是分别选择性拮抗葡萄糖和脂肪酸利用并刺激摄食的抗代谢药物。采用Fos免疫组织化学方法鉴定这些药物激活的脑神经元，并评估迷走神经在药物作用中的作用。远程静脉输注MA和2-DG诱导Fos样免疫反应（Fos-li）在特定的大脑部位，但模式是不同的两种药物。在孤束核（NTS）、臂旁外侧核中央亚核（IPBN）、杏仁中央核（CNA，外侧部）和迷走神经运动背核（DMV），巯基乙酸可诱导Fos-li的产生。迷走神经切断可完全阻断MA对脑内Fos-li的诱导作用。2-脱氧-D-葡萄糖也诱导NTS，CNA（外侧部分）和DMV，以及在外部IPBN亚核，蓝斑，下丘脑室旁核和视上核，并在整个间脑分散的细胞Fos-li。迷走神经切断不能阻断2-DG诱导Fos-li。结果表明，2-DG对Fos-li的作用是通过直接的中枢作用介导的，而MA的作用是通过外周感觉神经元介导的。因此，葡萄糖和脂肪酸的可用性通过不同的神经机制影响特定大脑部位的活动。Fos免疫反应位点与病变导致MA和2-DG诱导的摄食缺陷的位点的相关性表明，c-fos表达部分定义了参与摄食代谢控制的中枢途径。
2-Deoxy-D-glucose (2-DG) and 2-mercaptoacetate (MA) are antimetabolic drugs that selectively antagonize glucose and fatty acid utilization, respectively, and stimulate feeding. Fos immunohistochemistry was employed to identify brain neurons activated by these drugs and to assess the role of the vagus nerve in the drug effects. Remote intravenous infusions of both MA and 2-DG induced Fos-like immunoreactivity (Fos-li) in specific brain sites, but the pattern was different for the two drugs. Mercaptoacetate induced Fos-li in the nucleus of the solitary tract (NTS), the central subnucleus of the lateral parabrachial nucleus (IPBN), the central nucleus of the amygdala (CNA, lateral part) and the dorsal motor nucleus of the vagus (DMV). Induction of Fos-li in the brain by MA was totally abolished by vagotomy. 2-Deoxy-D-glucose also induced Fos-li in the NTS, CNA (lateral part) and DMV, as well as in the external IPBN subnucleus, locus coeruleus, paraventricular and supraoptic hypothalamic nuclei, and in scattered cells throughout the diencephalon. Induction of Fos-li by 2-DG was not blocked by vagotomy. Results suggest that 2-DG's effects on Fos-li are mediated by a direct central action, whereas MA's effects are mediated by peripheral sensory neurons. Thus, availability of glucose and fatty acids influences the activity of specific brain sites by different neural mechanisms. The correlation of Fos-immunoreactive sites with sites where lesions have been shown to cause deficits in MA- and 2-DG-induced feeding indicates that c-fos expression defines in part the central pathways involved in the metabolic control of feeding.