Ritter S, Hutton B
Department of Veterinary and Comparative Anatomy, Washington State University, Pullman 99164, USA.
Physiol Behav. 1995 Dec;58(6):1215-20. doi: 10.1016/0031-9384(95)02050-0.
Systemic administration of mercaptoacetate (MA) blocks beta oxidation of fatty acids and stimulates food intake. The present experiment examined MA-induced feeding in rats with bilateral lesions of the central nucleus of the amygdala (CNA) and sham-operated controls. Food intake was measured for 6 h immediately following i.p. injection of 400, 600, or 800 mumol/kg of MA or saline. Feeding was also measured in these rats in response to 2-deoxy-D-glucose (2DG) (100, 200, and 300 mg/kg, SC), a glucose analogue that competitively inhibits glucose utilization. We found that CNA lesions blocked feeding in response to all three doses of MA. Feeding in response to 2DG was significantly reduced, but not abolished, by the lesion. These findings suggest that the CNA is a crucial component of the neural pathway for feeding in response to MA and may also participate in 2DG-induced feeding.
巯基乙酸盐（MA）的全身给药会阻断脂肪酸的β氧化并刺激食物摄入。本实验研究了双侧杏仁核中央核（CNA）损伤的大鼠和假手术对照组中MA诱导的进食情况。腹腔注射400、600或800 μmol/kg的MA或生理盐水后，立即测量6小时内的食物摄入量。还测量了这些大鼠对2-脱氧-D-葡萄糖（2DG）（100、200和300 mg/kg，皮下注射）的进食反应，2DG是一种竞争性抑制葡萄糖利用的葡萄糖类似物。我们发现，CNA损伤会阻断对所有三种剂量MA的进食反应。损伤使对2DG的进食反应显著降低，但并未消除。这些发现表明，CNA是对MA进食反应的神经通路的关键组成部分，也可能参与2DG诱导的进食。
