Interactions of neuropeptide Y, hypocretin-I (orexin A) and melanin-concentrating hormone on feeding in rats.
Interactions of neuropeptide Y, hypocretin-I (orexin A) and melanin-concentrating hormone on feeding in rats.
复制标题
神经肽 Y、下丘脑分泌素-I（食欲素 A）和黑色素浓缩激素对大鼠喂养的相互作用。
DOI：
10.1016/s0006-8993(02)02941-4
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发表时间：
2002
期刊：
影响因子：
2.9
通讯作者：
Sahu,Abhiram
中科院分区：
文献类型：
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作者：
Sahu,Abhiram
在各种神经肽能系统中，神经肽Y （NPY）、下丘脑分泌素-1和黑色素浓缩激素（MCH）产生神经元已被证明在调节食物摄入和体重中发挥重要作用。所有这些神经肽都是促氧信号，最近的证据表明下丘脑这些神经元系统之间存在形态联系。然而，这些神经系统之间的功能相互作用尚不清楚。因此，在本研究中，我们研究了在大鼠第三次脑室注射（icv）后这些神经肽之间是否存在对食物摄入的协同作用。腹腔注射NPY（0.118、0.588、1.176 nmol）、下丘脑泌素-1 （1,3 nmol）和MCH（0.42、1.048、2.096 nmol）刺激小鼠摄食呈剂量依赖性。与单独注射NPY相比，共注射0.118 nmol的NPY和下丘脑泌素-1 （1,3 nmol）或MCH （0.42, 1.048, 2.096 nmol）对摄食量没有增加作用。而低剂量的NPY （0.023 nmol）和下丘脑泌素-1 （0.25 nmol）联合注射，单独注射效果不明显，但显著诱导了摄食。相比之下，低剂量的NPY （0.023 nmol）或下丘脑泌素-1 （0.25 nmol）与低剂量的MCH（0.21、0.42 nmol）联合使用，与单独使用MCH相比，并没有导致食物摄入量进一步增加。此外，0.25 nmol下丘脑泌素-1和非刺激性剂量的MCH （0.105 nmol）联合使用对刺激食物摄入无效。最后，与生理盐水对照组相比，共注射0.023 NPY和0.105 nmol MCH显著诱导了食物摄入，但与NPY或MCH处理组相比没有显著差异。总的来说，这些结果表明(1)NPY和下丘脑分泌素-1之间有协同作用，(2)下丘脑分泌素-1和MCH之间没有相互作用，(3)NPY和MCH在诱导食物摄入方面几乎没有相互作用。综上所述，这些结果为NPY和下丘脑分泌素神经元之间的形态学联系提供了生理上的支持，表明这两个摄氧信号在控制食物摄入方面存在相互作用，并进一步表明MCH对摄食的作用可能独立于NPY和下丘脑分泌素-1的作用。
Amongst various neuropeptidergic systems, neuropeptide Y (NPY), hypocretin-1 and melanin-concentrating hormone (MCH) producing neurons have been shown to play an important role in the regulation of food intake and body weight. All of these neuropeptides are orexigenic signals and recent evidence suggests the existence of morphological connections between these neuronal systems in the hypothalamus. However, the functional interactions between these neuronal systems are not clearly understood. Therefore, in the present study, we examined whether there is a cooperative action on food intake between these neuropeptides after third intracerebroventricular (icv) injection in the rat. The icv administration of NPY (0.118, 0.588, 1.176 nmol), hypocretin-1 (1, 3 nmol) and MCH (0.42, 1.048, 2.096 nmol) stimulated food intake in a dose dependent manner. Coinjection with 0.118 nmol of NPY and hypocretin-1 (1, 3 nmol) or MCH (0.42, 1.048, 2.096 nmol) had no additive effect on food intake as compared to that of NPY alone. However, coinjection with lower dose of NPY (0.023 nmol) and hypocretin-1 (0.25 nmol), that did not have any effect alone, significantly induced food intake. In contrast, combination of a lower dose of NPY (0.023 nmol) or hypocretin-1 (0.25 nmol) with lower stimulatory dose (0.21, 0.42 nmol) of MCH did not result in further increase in food intake as compared to that of MCH alone. Also, combination of 0.25 nmol hypocretin-1 and a non-stimulatory dose of MCH (0.105 nmol) was ineffective in stimulating food intake. Finally, coinjection with of 0.023 nmol NPY and 0.105 nmol MCH significantly induced food intake as compared to saline control group but not as compared to NPY or MCH treated groups. In total, these results show (1) a synergistic action between NPY and hypocretin-1, (2) no interaction between hypocretin-1 and MCH and (3) very little interaction, if any, between NPY and MCH in inducing food intake. In conclusion, these results provide a physiological concomitant to the previous demonstration of morphological contacts between NPY and hypocretin producing neurons by suggesting an interaction between these two orexigenic signals in control of food intake, and further suggest that MCH’s action on feeding may be independent of NPY and hypocretin-1 action.