Gosnell B A, Morley J E, Levine A S, Kneip J, Frick M, Elde R P
Physiol Behav. 1984 Jul;33(1):27-30. doi: 10.1016/0031-9384(84)90008-8.
It has been shown that spreading depression of the hippocampus can elicit feeding, and that several opioid peptides elicit spreading depression when injected into the hippocampus. To determine whether such depression is the primary mechanism by which opiates induce feeding, we tested the feeding effects of naloxone, an opiate antagonist, and butorphanol tartrate, a kappa-sigma agonist, on feeding in rats with and without hippocampal lesions. Naloxone tended to reduce intake approximately equally in the two groups. Similarly, the doses of butorphanol that increased intake in sham rats were equally effective in lesioned rats. It was concluded that the hippocampus is not the major structure mediating opiate-induced feeding.
研究表明，海马体的扩散性抑制可引发进食，并且几种阿片肽注入海马体时可引发扩散性抑制。为了确定这种抑制是否是阿片类药物诱导进食的主要机制，我们测试了阿片类拮抗剂纳洛酮和κ-σ激动剂酒石酸布托啡诺对有或没有海马体损伤的大鼠进食的影响。纳洛酮在两组中倾向于同等程度地减少摄入量。同样，在假手术大鼠中增加摄入量的酒石酸布托啡诺剂量在损伤大鼠中同样有效。得出的结论是，海马体不是介导阿片类药物诱导进食的主要结构。
