Arjune D, Bodnar R J
Department of Psychology and Neuropsychology Doctoral Sub-Program Queens College, City University of New York, Flushing 11367.
Brain Res Bull. 1990 Mar;24(3):375-9. doi: 10.1016/0361-9230(90)90092-e.
Central administration of alloxan reduces the hyperphagic, but not the hyperglycemic response to glucoprivation by presumably acting upon brain glucoreceptors or a glucoprivic control mechanism. The present study evaluated whether central alloxan pretreatment respectively altered the dose-dependent suppressant effects upon deprivation (24-hr)-induced feeding of naloxone (0.01-10 mg/kg, IP) and cholecystokinin octapeptide (CCK-8: 1-8 micrograms/kg, IP) in rats. Central alloxan (200 micrograms, ICV) failed to alter body weight, free-feeding and deprivation-induced feeding. Both naloxone and CCK-8 produced significant dose-dependent inhibitions of deprivation-induced feeding in control rats. Central alloxan treatment significantly diminished peak naloxone hypophagia induced by 2.5 and 10 mg/kg doses, and CCK-8 hypophagia induced by the 1 and 4 micrograms/kg doses. Coadministration of 3 M D-glucose, which acts as a cytoprotectant against alloxan-induced diabetes, blocked the attenuating actions of alloxan upon naloxone and CCK-8 hypophagia. These data indicate the effectiveness of central alloxan in restricting the ability of pharmacological agents to either stimulate or inhibit food intake in rats without altering basal intake or body weight maintenance.
四氧嘧啶的中枢给药通过作用于脑葡萄糖受体或葡萄糖缺乏控制机制，减少了对葡萄糖缺乏的摄食亢进反应，但未减少高血糖反应。本研究评估了中枢四氧嘧啶预处理是否分别改变了纳洛酮（0.01 - 10毫克/千克，腹腔注射）和八肽胆囊收缩素（CCK - 8：1 - 8微克/千克，腹腔注射）对大鼠禁食（24小时）诱导摄食的剂量依赖性抑制作用。中枢四氧嘧啶（200微克，脑室内注射）未能改变体重、自由摄食和禁食诱导的摄食。纳洛酮和CCK - 8均对对照大鼠禁食诱导的摄食产生显著的剂量依赖性抑制。中枢四氧嘧啶处理显著减弱了2.5和10毫克/千克剂量的纳洛酮引起的摄食减少峰值，以及1和4微克/千克剂量的CCK - 8引起的摄食减少峰值。作为四氧嘧啶诱导糖尿病细胞保护剂的3 M D - 葡萄糖的共同给药，阻断了四氧嘧啶对纳洛酮和CCK - 8摄食减少的减弱作用。这些数据表明中枢四氧嘧啶在不改变基础摄食或体重维持的情况下，限制了药物刺激或抑制大鼠食物摄入能力的有效性。
