Burns G A, Ritter R C
Department of VCAPP, College of Veterinary Medicine, Washington State University, Pullman 99164-6520, USA.
Pharmacol Biochem Behav. 1997 Jan;56(1):145-9. doi: 10.1016/S0091-3057(96)00171-2.
A role for excitatory amino acids in the control of feeding behavior has not been extensively investigated. Nevertheless, there is direct and circumstantial evidence to indicate that some circuits involved with feeding behavior include glutamatergic elements. To test the hypothesis that endogenous glutamate participates in the control of food intake, we performed experiments to determine whether MK-801, a non-competitive N-methyl-D-aspartate (NMDA) ion channel antagonist, is capable of altering intake of liquid and solid foods in hungry or satiated rats. Following a 16 h fast, intake of 15% sucrose was significantly enhanced by systemic treatment with MK-801. Water intake was not altered by the NMDA antagonist. Rats did not ingest more rat chow after MK-801, unless they had been fasted. When a more palatable food (cookies) was offered, MK-801 did increase intake. Thus MK-801 enhanced food intake only when feeding was initiated by food-deprivation or increased palatability. In conclusion, our results support the hypothesis that endogenous glutamate plays a role in the control of food intake. Blockade of NMDA receptor function by MK-801 may diminish or delay satiety signals, rather than initiate feeding behavior per se.
兴奋性氨基酸在进食行为控制中的作用尚未得到广泛研究。然而，有直接和间接证据表明，一些与进食行为相关的神经回路包含谷氨酸能成分。为了验证内源性谷氨酸参与食物摄入控制这一假说，我们进行了实验，以确定非竞争性N-甲基-D-天冬氨酸（NMDA）离子通道拮抗剂MK-801是否能够改变饥饿或饱腹大鼠的液体和固体食物摄入量。禁食16小时后，MK-801全身给药可显著增加15%蔗糖的摄入量。NMDA拮抗剂未改变水的摄入量。MK-801给药后，大鼠除非禁食，否则不会摄入更多大鼠饲料。当提供更美味的食物（饼干）时，MK-801确实会增加摄入量。因此，只有在因食物剥夺或适口性增加而开始进食时，MK-801才会增加食物摄入量。总之，我们的结果支持内源性谷氨酸在食物摄入控制中起作用这一假说。MK-801对NMDA受体功能的阻断可能会减弱或延迟饱腹感信号，而不是引发进食行为本身。
