Kyrkouli S E, Stanley B G, Hutchinson R, Seirafi R D, Leibowitz S F
Rockefeller University, New York, NY 10021.
Brain Res. 1990 Jun 25;521(1-2):185-91. doi: 10.1016/0006-8993(90)91541-n.
The neuropeptide galanin (GAL) has been found to elicit feeding after injection into the paraventricular hypothalamic nucleus (PVN), where it coexists with norepinephrine (NE), a neurotransmitter believed to be important in the control of natural feeding behavior. Using pharmacological tools, this study investigated the possibility that PVN GAL influences food intake via its direct interaction with the noradrenergic system localized in this nucleus. Tests with alpha-adrenergic receptor blockers demonstrated that GAL-induced feeding, similar to NE-stimulated feeding, depends specifically upon functional alpha 2-receptor sites. Further, experimentation with the catecholamine synthesis inhibitors, alpha-methyl-p-tyrosine and Fla-63, suggested that GAL's action also depends upon the release of endogenous NE. This is in contrast to another hypothalamic peptide, neuropeptide Y, which is also a strong stimulant of food intake and coexists with NE in the PVN. Neuropeptide Y remains effective in eliciting feeding in the presence of alpha 2-receptor antagonists and catecholamine-synthesis inhibitors, suggesting that, unlike GAL, it can act independently of endogenous NE.
已发现神经肽甘丙肽(GAL)注入下丘脑室旁核(PVN)后会引发进食行为,在该核中它与去甲肾上腺素(NE)共存,而去甲肾上腺素是一种据信在控制自然进食行为中起重要作用的神经递质。本研究利用药理学工具,探究了PVN中的GAL是否通过与该核中的去甲肾上腺素能系统直接相互作用来影响食物摄入。用α-肾上腺素能受体阻滞剂进行的测试表明,GAL诱导的进食,与NE刺激的进食相似,特别依赖于功能性α2-受体位点。此外,用儿茶酚胺合成抑制剂α-甲基对酪氨酸和Fla-63进行的实验表明,GAL的作用也依赖于内源性NE的释放。这与另一种下丘脑肽神经肽Y形成对比,神经肽Y也是食物摄入的强烈刺激剂,且与NE在PVN中共存。在存在α2-受体拮抗剂和儿茶酚胺合成抑制剂的情况下,神经肽Y在引发进食方面仍然有效,这表明,与GAL不同,它可以独立于内源性NE发挥作用。