Tordoff M G, Geiselman P J, Grijalva C V, Kiefer S W, Novin D
Am J Physiol. 1982 Jan;242(1):R129-35. doi: 10.1152/ajpregu.1982.242.1.R129.
Bilateral lesions of the amygdala in male rats impaired the feeding response to 2-deoxy-D-glucose (2-DG; 100, 200, and 400 mg/kg). During the first 3 h postinjection, control rats displayed a dose-related increase in both food and water consumption. Rats with amygdaloid lesions did not respond to 2-DG until the 3rd h postinjection, when only the two largest doses significantly increased food consumption. Their water intake remained unaffected throughout the 3-h postinjection period. During the 4th-24th h post-2-DG administration, both groups displayed a dose-related suppression of food and water intake. Following insulin (10 U/kg), amygdaloid and control animals were indistinguishable: both groups showed a significant short-term increase in food and water intake followed by a reduction in intakes during the 4th-24th h. Central visceral pathways that are important for the ingestive responses to 2-DG may be interrupted by amygdaloid lesions. However, pathways responsible for the ingestive behavior induced by insulin appear unaffected by damage to the amygdala.
雄性大鼠双侧杏仁核损伤会损害其对2-脱氧-D-葡萄糖(2-DG;100、200和400毫克/千克)的进食反应。在注射后最初3小时内,对照大鼠的食物和水消耗量均呈现剂量相关的增加。杏仁核损伤的大鼠直到注射后第3小时才对2-DG产生反应,此时只有两个最大剂量显著增加了食物消耗量。在注射后3小时内,它们的水摄入量未受影响。在给予2-DG后的第4至24小时内,两组的食物和水摄入量均呈现剂量相关的抑制。注射胰岛素(10单位/千克)后,杏仁核损伤组和对照组动物没有区别:两组均在短期内食物和水摄入量显著增加,随后在第4至24小时摄入量减少。对2-DG摄食反应重要的中枢内脏通路可能被杏仁核损伤中断。然而,负责胰岛素诱导摄食行为的通路似乎不受杏仁核损伤的影响。