Neuropeptide W acts in brain to control prolactin, corticosterone, and growth hormone release

Neuropeptide W acts in brain to control prolactin, corticosterone, and growth hormone release
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DOI:
10.1210/en.2002-0161
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发表时间:
2003-07-01
期刊:
影响因子:
4.8
通讯作者:
Samson, WK
Samson, WK
中科院分区:
医学2区
文献类型:
--
作者:
Baker, JR;Cardinal, K;Samson, WK

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孤儿受体GPR7和GPR8的内源性多肽配体被鉴定为神经肽W(NPW)。因为这些受体在大脑中表达,特别是在下丘脑,我们假设NPW可能与神经内分泌系统相互作用,神经内分泌系统控制垂体前叶的激素释放。当NPW与分散的垂体前叶细胞孵育时,NPW对催乳素(PRL)、ACTH或GH的体外释放没有显著影响。然而,当NPW以剂量相关的方式注射到清醒的无拘束的雄性大鼠的侧脑室时,升高了PRL和皮质酮,降低了循环中的GH水平。三种效应的阈值剂量均为1.0nmol。我们的结论是,内源性NPW可能在神经内分泌信号进入垂体前叶的组织中起调节作用,但本身并不是腺体内真正的释放或抑制因子。中央对NPW23的管理也刺激了饮用水和食物的摄入量。外源性多肽降低GH但刺激PRL分泌和激活下丘脑-垂体肾上腺轴的能力,以及观察到的行为效应,提示内源性NPW可能在下丘脑对应激的反应中发挥作用。
The endogenous, peptide ligand for the orphan receptors GPR7 and GPR8 was identified to be neuropeptide W (NPW). Because these receptors are expressed in brain and in particular in hypothalamus, we hypothesized that NPW might interact with neuroendocrine systems that control hormone release from the anterior pituitary gland. No significant effects of NPW were observed on the in vitro releases of prolactin (PRL), ACTH, or GH when log molar concentrations ranging from 1 pM to 100 nM NPW were incubated with dispersed anterior pituitary cells. However, NPW, when injected into the lateral cerebroventricle of conscious, unrestrained male rats, in a dose-related fashion elevated PRL and corticosterone and lowered GH levels in circulation. The threshold dose for all three effects was 1.0 nmol. We conclude that endogenous NPW may play a regulatory role in the organization of neuroendocrine signals accessing the anterior pituitary gland but does not itself act as a true releasing or inhibiting factor in the gland. Central administration of NPW23 also stimulated water drinking and food intake. The ability of exogenous peptide to decrease GH but stimulate PRL secretion and activate the hypothalamo-pituitary adrenal axis, together with the observed behavioral effects, suggests that endogenous NPW may play a role in the hypothalamic response to stress.