Antinociceptive effects of neuropeptide Y and related peptides in mice
Antinociceptive effects of neuropeptide Y and related peptides in mice
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DOI：
10.1016/0006-8993(96)00262-4
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发表时间：
1996-06-10
期刊：
影响因子：
2.9
通讯作者：
Dahl, SG
中科院分区：
文献类型：
--
作者：
Broqua, P;Wettstein, JG;Dahl, SG
本研究比较了小鼠侧脑室给药后NPY及其类似物的抗伤害性和促食欲活性。NPY在小鼠扭体试验中具有抗伤害性作用，其不受用纳洛酮的Drier处理的影响。育亨宾、咪唑克生或利血平。详细的检查显示，NPY（0.023-0.7 nmol）、PYY（0.007-0.07 nmol）、NPY 2 -36（0.023-0.23 nmol）和Y-1激动剂[Leu（31），Pro（34）]-NPY（0.07-0.7 nmol）都产生了剂量依赖性的和完全的对乙酸诱导的扭体的抑制。相比之下，Y-2激动剂NPY 13 -26具有很少或没有抗伤害感受作用。如它们的艾德（50）值所示，肽的相对效力为PYY > NPY 2 -36大于或等于NPY > [Leu（31），Pro（34）]-NPY远大于NPY 13 -36，表明Y-1而不是Y-2或Y-3受体亚型参与抗伤害感受作用。此后，评估所有肽对食物摄入的影响。在剂量和肽特异性方面，NPY和相关肽的吞噬作用与伤害性感受的吞噬作用相同，提示了共同的受体机制。然而，一种据称的NPY拮抗剂，[D-Trp（32）]-NPY，减弱了NPY对进食的影响，然而这种相同的肽引起了对乙酸诱导的扭体的剂量依赖性抑制，表明抗伤害感受和刺激食物摄入之间的一些分子区别。
This study compares the antinociceptive and orexigenic activities of NPY and analogs after intracerebroventricular administration in mice. NPY had an antinociceptive action in the mouse writhing test which was not affected by Drier treatment with naltrexone. yohimbine, idazoxan or reserpine. A detailed examination revealed that NPY (0.023-0.7 nmol), PYY (0.007-0.07 nmol), NPY2-36 (0.023-0.23 nmol) and the Y-1 agonist [Leu(31),Pro(34)]-NPY (0.07-0.7 nmol) all produced a dose-dependent and complete suppression of acetic acid-induced writhing. In contrast, the Y-2 agonist, NPY13-26, had little or no antinociceptive effect. As shown by their ED(50) values, the relative potency of the peptides was PYY > NPY2-36 greater than or equal to NPY > [Leu(31),Pro(34)]-NPY much greater than NPY13-36, suggesting that a Y-1 rather than a Y-2 or Y-3 receptor subtype was implicated in the antinociceptive action. Thereafter, all peptides were assessed for their effects on food intake. With respect to dose and peptide specificity, the hyperphagic effects of NPY and related peptides paralleled those on nociception, suggesting a common receptor mechanism. However, a purported NPY antagonist, [D-Trp(32)]-NPY, attenuated NPY's effect on feeding yet this same peptide elicited a dose-dependent inhibition of acetic acid-induced writhing, suggesting some molecular distinction between antinociception and stimulation of food intake.