Reduction in adiposity affects the extent of afferent projections to growth hormone-releasing hormone and somatostatin neurons and the degree of colocalization of neuropeptides in growth hormone-releasing hormone and somatostatin cells of the ovine hypothalamus
Reduction in adiposity affects the extent of afferent projections to growth hormone-releasing hormone and somatostatin neurons and the degree of colocalization of neuropeptides in growth hormone-releasing hormone and somatostatin cells of the ovine hypothalamus
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DOI：
10.1210/en.2005-0622
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发表时间：
2005-11-01
期刊：
影响因子：
4.8
通讯作者：
Clarke, IJ
中科院分区：
文献类型：
--
作者：
Iqbal, J;Manley, TR;Clarke, IJ
各种神经肽和神经递质通过作用于GHRH和生长抑素（SRIF）细胞影响生长激素的分泌。生长激素分泌也受到肥胖改变的影响，这可能是通过调节GHRH和SRIF细胞。我们量化了瘦肉羊（限食羊）和正常饲养羊（n = 4/组）GHRH和SRIF细胞中神经肽的共定位以及对这些细胞的传入投射。瘦肉动物弓形核中ghrh免疫反应（IR）细胞数量较多，但两组脑室周围核中SRIF- IR细胞数量相似。GHRH- IR细胞亚群在瘦肉动物中定位神经肽Y，但在正常喂养的动物中未见。GHRH/ gal丙氨酸（GAL）共定位在瘦肉动物中更高，但GHRH/酪氨酸羟化酶或GHRH/ GAL样肽细胞的数量没有差异。SRIF/脑啡肽共定位在瘦肉动物中较低。在瘦肉和正常喂养的动物中，接受SRIF输入的GHRH神经元的百分比相似，但在正常喂养的动物中，更多的GHRH细胞接受脑啡肽传入的输入。在瘦肉动物中，接受GHRH、神经肽Y、GAL和食欲素传入的SRIF细胞百分比更高。这些发现为食欲调节肽和多巴胺调节生长激素分泌的中枢机制提供了解剖学证据。瘦肉动物增加对SRIF细胞的输入可能抑制和允许生长激素的增加。瘦动物GHRH细胞中NPY的出现可能是调节GH分泌增加与肥胖减少的机制。
Various neuropeptides and neurotransmitters affect GH secretion by acting on GHRH and somatostatin ( SRIF) cells. GH secretion is also affected by alteration in adiposity, which could be via modulation of GHRH and SRIF cells. We quantified colocalization of neuropeptides in GHRH and SRIF cells and afferent projections to these cells in lean ( food restricted) and normally fed sheep ( n = 4/ group). The number of GHRH-immunoreactive ( IR) cells in the arcuate nucleus was higher in lean animals, but the number of SRIF- IR cells in the periventricular nucleus was similar in the two groups. A subpopulation of GHRH- IR cells colocalized neuropeptide Y in lean animals, but this was not seen in normally fed animals. GHRH/ galanin ( GAL) colocalization was higher in lean animals with no difference in numbers of GHRH/ tyrosine hydroxylase ylase or GHRH/ GAL- like peptide cells. SRIF/ enkephalin colocalization was lower in lean animals. The percentage of GHRH neurons receiving SRIF input was similar in lean and normally fed animals, but more GHRH cells received input from enkephalin afferents in normally fed animals. The percentage of SRIF cells receiving GHRH, neuropeptide Y, GAL, and orexin afferents was higher in lean animals. These findings provide an anatomical evidence of central mechanism( s) by which appetite- regulating peptides and dopamine could regulate GH secretion. Increased input to SRIF cells in lean animals may be inhibitory and permissive of increased GH. The appearance of NPY in GHRH cells of lean animals may be a mechanism for regulation of increasing GH secretion with reduced adiposity.