Ritter S, Taylor J S
Department of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, Washington State University, Pullman 99164-6520.
Am J Physiol. 1990 Jun;258(6 Pt 2):R1395-401. doi: 10.1152/ajpregu.1990.258.6.R1395.
This experiment examined the role of subdiaphragmatic vagal sensory neurons in feeding stimulated by pharmacological blockade of fatty-acid oxidation (lipoprivic feeding) and glucose utilization (glucoprivic feeding). Rats prepared by surgical transection of the subdiaphragmatic vagal trunk or aspiration lesion of the vagal sensory terminal fields in the area postrema-nucleus of the solitary tract (AP-NTS) were maintained and tested on a fat-supplemented, high carbohydrate diet. Fatty-acid oxidation was blocked with mercaptoacetate (MA, 400 and 600 mumol/kg ip) and glucose utilization was blocked with 2-deoxy-D-glucose (2-DG, 100 and 200 mg/kg sc). On test days, rats were injected with MA, 2-DG, or saline, and feeding was measured hourly for 6 h beginning immediately after injection. We found that both subdiaphragmatic vagotomy and AP-NTS lesions abolished lipoprivic feeding. In contrast, glucoprivic feeding was abolished by AP-NTS lesions but not by subdiaphragmatic vagotomy. These results indicate that lipoprivic feeding requires intact subdiaphragmatic vagal sensory neurons that terminate in the AP-NTS region. Glucoprivic feeding is not vagally mediated but also requires a neural substate within the AP-NTS region.
本实验研究了膈下迷走神经感觉神经元在脂肪酸氧化药理学阻断（脂肪缺乏性摄食）和葡萄糖利用阻断（糖缺乏性摄食）所刺激的摄食过程中的作用。通过手术横断膈下迷走神经干或损毁孤束核最后区（AP-NTS）内迷走神经感觉终末区域制备的大鼠，维持在补充脂肪的高碳水化合物饮食上并进行测试。用巯基乙酸盐（MA，腹腔注射400和600 μmol/kg）阻断脂肪酸氧化，用2-脱氧-D-葡萄糖（2-DG，皮下注射100和200 mg/kg）阻断葡萄糖利用。在测试日，给大鼠注射MA、2-DG或生理盐水，注射后立即开始每小时测量6小时的摄食量。我们发现膈下迷走神经切断术和AP-NTS损毁均消除了脂肪缺乏性摄食。相反，糖缺乏性摄食被AP-NTS损毁消除，但未被膈下迷走神经切断术消除。这些结果表明，脂肪缺乏性摄食需要完整的、终止于AP-NTS区域的膈下迷走神经感觉神经元。糖缺乏性摄食不是由迷走神经介导的，但也需要AP-NTS区域内的一种神经状态。
