کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4326394 | 1614075 | 2010 | 11 صفحه PDF | دانلود رایگان |
Puberty in primates is first delayed by a neurobiological switch that arrests pulsatile GnRH release during infancy and then triggered, after a protracted period of juvenile development, by resurgence in intermittent release of this hypothalamic peptide. The purpose of this chapter is to review recent studies conducted in our laboratories to begin to examine the role of thyroid hormone (TH) in governing this postnatal development of pulsatile GnRH release in primates and therefore the timing of puberty in these species. The male rhesus monkey was used as the experimental model and TH activity was manipulated by surgical and chemical thyroidectomy on the one hand, and by thyroxine (T4) and triiodothyronine (T3) replacement on the other. Our results indicate that the resurgence in pulsatile GnRH release at the termination of the juvenile phase of development is dependent on a permissive action of TH. Whether this action of TH is mediated directly on hypothalamic centers regulating the pulsatile release of GnRH, or indirectly by circulating signals reflecting TH action on somatic development remains to be determined.
Research highlights
► Pubertal reactivation of GnRH release in monkeys depends on permissive action of TH.
► TH deficit in infancy did not alter shut-off or pubertal turn-on of GnRH release.
► Delay in puberty by juvenile hypothyroidism is linked to retarded growth.
► Whether TH action is direct on CNS or indirect via a somatic signal is unknown.
Journal: Brain Research - Volume 1364, 10 December 2010, Pages 175–185