Central neuropeptide B administration activates stress hormone secretion and stimulates feeding in male rats
Central neuropeptide B administration activates stress hormone secretion and stimulates feeding in male rats
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DOI：
10.1111/j.1365-2826.2004.01239.x
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发表时间：
2004-10-01
影响因子：
3.2
通讯作者：
Taylor, MM
中科院分区：
文献类型：
--
作者：
Samson, WK;Baker, JR;Taylor, MM
神经肽 B (NPB) 被鉴定为孤儿受体 GPR7 和 GPR8 的内源性肽配体。由于 GPR7 在大鼠大脑中表达，特别是在下丘脑中表达，我们假设 NPB 可能与控制垂体前叶释放激素的神经内分泌系统相互作用。当对数摩尔浓度范围为 1 pM 至 100 nM NPB 与从雄性大鼠采集的分散的垂体前叶细胞一起孵育时，未观察到 NPB 对催乳素、促肾上腺皮质激素 (ACTH) 或生长激素 (GH) 的体外释放有显着影响。此外，NPB (100 nM) 不会改变促甲状腺激素释放激素对催乳素分泌、促肾上腺皮质激素释放因子(CRF) 引起的 ACTH 分泌和 GH 释放激素引起的 GH 分泌的浓度反应刺激。然而，当将 NPB 注射到有意识、不受约束的雄性大鼠的侧脑室 (i.c.v.) 时，会升高催乳素和皮质酮，并降低循环中的 GH 水平。对皮质酮和催乳素水平产生影响的阈剂量为 1.0 nmol，而对 GH 释放产生影响的阈剂量为 3.0 nmol NPB。用多克隆抗CRF抗血清进行预处理，完全阻断了NPB刺激ACTH释放的能力，并显着抑制了NPB对血浆皮质酮水平的影响。 NPB 管理 i.c.v.没有显着改变清醒大鼠的血浆加压素和催产素水平。它确实以类似于 GPR7 的另一种内源性配体神经肽 W 的方式刺激饱腹动物的摄食（最小有效剂量 1.0 nmol）。我们得出的结论是，NPB 可以在大脑中发挥作用，调节进入垂体前叶的神经内分泌信号，但本身并不充当腺体中的释放或抑制因子，至少在催乳素、ACTH 和 GH 分泌方面。
Neuropeptide B (NPB) was identified to be an endogenous, peptide ligand for the orphan receptors GPR7 and GPR8. Because GPR7 is expressed in rat brain and, in particular, in the hypothalamus, we hypothesized that NPB might interact with neuroendocrine systems that control hormone release from the anterior pituitary gland. No significant effects of NPB were observed on the in vitro releases of prolactin, adrenocorticotropic hormone (ACTH) or growth hormone (GH) when log molar concentrations ranging from 1 pM to 100 nM NPB were incubated with dispersed anterior pituitary cells harvested from male rats. In addition NPB (100 nM) did not alter the concentration response stimulation of prolactin secretion by thyrotropin-releasing hormone, ACTH secretion by corticotropin-releasing factor (CRF) and GH secretion by GH-releasing hormone. However, NPB, when injected into the lateral cerebroventricle (i.c.v.) of conscious, unrestrained male rats, elevated prolactin and corticosterone, and lowered GH levels in circulation. The threshold dose for the effect on corticosterone and prolactin levels was 1.0 nmol, while that for the effect on GH release was 3.0 nmol NPB. Pretreatment with a polyclonal anti-CRF antiserum completely blocked the ability of NPB to stimulate ACTH release and significantly inhibited the effect of NPB on plasma corticosterone levels. NPB administration i.c.v. did not significantly alter plasma vasopressin and oxytocin levels in conscious rats. It did stimulate feeding (minimum effective dose 1.0 nmol) in sated animals in a manner similar to that of the other endogenous ligand for GPR7, neuropeptide W. We conclude that NPB can act in the brain to modulate neuroendocrine signals accessing the anterior pituitary gland, but does not itself act as a releasing or inhibiting factor in the gland, at least with regard to prolactin, ACTH and GH secretion.