Aja S M, Barrett J A, Gietzen D W
Department of Veterinary Medicine: Anatomy, Physiology and Cell Biology, University of California-Davis, 95616-8732, USA.
Pharmacol Biochem Behav. 1999 Mar;62(3):487-91. doi: 10.1016/s0091-3057(98)00212-3.
Serotonin3 (5-HT3) receptors in the periphery mediate anorectic responses to the amino acid deficiency, which occurs after eating amino acid-imbalanced diets (IMB). However, other neurochemical systems, notably cholecystokinin (CCK), are known to affect food intake. We pretreated rats systemically with tropisetron, a 5-HT3 receptor antagonist, alone and combined with antagonists of CCK(A) and CCK(B) receptors, and measured intake of an IMB. Devazepide, a CCK(A) receptor antagonist, appeared to interact with tropisetron in the anorectic responses to IMB, blunting the usual remediation of IMB anorexia by tropisetron. The CCK(B) receptor antagonist, L-365, 260, increased intake of both IMB and an amino acid-balanced basal diet (BAS) and did not interact with tropisetron. Our data suggest that activation of CCK(A) receptors is interactive with 5-HT3 receptor activity in mediating IMB anorexia in the aminoprivic feeding model.
外周的5-羟色胺3（5-HT3）受体介导对氨基酸缺乏的厌食反应，这种氨基酸缺乏发生在摄入氨基酸不平衡饮食（IMB）之后。然而，已知其他神经化学系统，尤其是胆囊收缩素（CCK），会影响食物摄入量。我们分别用5-HT3受体拮抗剂托烷司琼对大鼠进行全身预处理，并将其与CCK（A）和CCK（B）受体拮抗剂联合使用，然后测量IMB的摄入量。CCK（A）受体拮抗剂地伐西匹在对IMB的厌食反应中似乎与托烷司琼相互作用，减弱了托烷司琼对IMB厌食症通常的改善作用。CCK（B）受体拮抗剂L-365,260增加了IMB和氨基酸平衡基础饮食（BAS）的摄入量，且不与托烷司琼相互作用。我们的数据表明，在氨基缺乏喂养模型中，CCK（A）受体的激活在介导IMB厌食症方面与5-HT3受体活性相互作用。
