Title of article :
Synthesis and secretion of GnRH
Author/Authors :
Clarke، نويسنده , , Iain J. and Pompolo، نويسنده , , Sueli، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2005
Pages :
27
From page :
29
To page :
55
Abstract :
Comprehensive studies have provided a clear understanding of the effects of gonadal steroids on the secretion of gonadotropin releasing hormone (GnRH), but some inconsistent results exist with regard to effects on synthesis. It is clear that regulation of both synthesis and the secretion of GnRH are effected by neurotransmitter systems in the brain. Thus, steroid regulation of GnRH synthesis and secretion can be direct, but the predominant effects are transmitted through steroid-responsive neuronal systems in various parts of the brain. There is also emerging evidence of direct effects on GnRH cells. Overriding effects on synthesis and secretion of GnRH can be observed during aging, in undernutrition and under stressful situations; these involve various neuronal systems, which may have serial or parallel effects on GnRH cells. The effect of aging is accompanied by changes in GnRH synthesis, but comprehensive studies of synthesis during undernutrition and stress are less well documented. Altered GnRH and gonadotropin secretion that occurs in seasonal breeding animals and during the pubertal transition is not generally accompanied by changes in GnRH synthesis. Secretion of GnRH from the brain is a reflection of the inherent function of GnRH cells and the inputs that integrate all of the central regulatory elements. Ultimately, the pattern of secretion dictates the reproductive status of the organism. In order to fully understand the central mechanisms that control reproduction, more extensive studies are required on the neuronal circuitry that provides input to GnRH cells.
Keywords :
Gonadotropins , Reproduction , neuroendocrinology , Estrogen , GNRH
Journal title :
Animal Reproduction Science
Serial Year :
2005
Journal title :
Animal Reproduction Science
Record number :
1908484
Link To Document :
بازگشت