Corticotrophin-releasing factor and stress-induced inhibition of the gonadotrophin-releasing hormone pulse generator in the female

TY - JOUR

T1 - Corticotrophin-releasing factor and stress-induced inhibition of the gonadotrophin-releasing hormone pulse generator in the female

AU - Li, X. F.

AU - Knox, A. M. I.

AU - O'Byrne, Kevin

PY - 2010/12/10

Y1 - 2010/12/10

N2 - It is well established that stress activates the hypothalamo-pituitary-adrenal (HPA) axis and suppresses the hypothalamo-pituitary-gonadal (HPG) axis A large literature dealing with various stressors that regulate gonadotrophin releasing hormone (GnRH) secretion in a variety of species (including nonhuman primates sheep and rats) provides evidence that stress modulates GnRH secretion by activating the corticotrophin releasing factor (CRF) system and sympathoadrenal pathways as well as the limbic brain Different stressors may suppress the HPG axis by activating or inhibiting various pathways in the CNS In addition to CRF being the principal hypophysiotropic factor driving the HPA axis, it is a potent inhibitor of the GnRH pulse generator The suppression of the GnRH pulse generator by a variety of stressful stimuli can be blocked by CRF antagonists, suggesting a pivotal role for endogenous CRF The differential roles for CRF receptor type 1 (CRF R1) and CRF R2 in stress induced suppression of the GnRH pulse generator add to the complexity of CRF regulation of the HPG axis Although the precise sites and mechanisms of action remain to be elucidated noradrenergic and gamma amino butyric acid (GABA) neurones are implicated in the system s regulation and opioids and kisspeptin in the medial preoptic area (mPOA) and hypothalamic arcuate nucleus (ARC) may operate downstream of the CRF neuronal system (C) 2010 Published by Elsevier B V

AB - It is well established that stress activates the hypothalamo-pituitary-adrenal (HPA) axis and suppresses the hypothalamo-pituitary-gonadal (HPG) axis A large literature dealing with various stressors that regulate gonadotrophin releasing hormone (GnRH) secretion in a variety of species (including nonhuman primates sheep and rats) provides evidence that stress modulates GnRH secretion by activating the corticotrophin releasing factor (CRF) system and sympathoadrenal pathways as well as the limbic brain Different stressors may suppress the HPG axis by activating or inhibiting various pathways in the CNS In addition to CRF being the principal hypophysiotropic factor driving the HPA axis, it is a potent inhibitor of the GnRH pulse generator The suppression of the GnRH pulse generator by a variety of stressful stimuli can be blocked by CRF antagonists, suggesting a pivotal role for endogenous CRF The differential roles for CRF receptor type 1 (CRF R1) and CRF R2 in stress induced suppression of the GnRH pulse generator add to the complexity of CRF regulation of the HPG axis Although the precise sites and mechanisms of action remain to be elucidated noradrenergic and gamma amino butyric acid (GABA) neurones are implicated in the system s regulation and opioids and kisspeptin in the medial preoptic area (mPOA) and hypothalamic arcuate nucleus (ARC) may operate downstream of the CRF neuronal system (C) 2010 Published by Elsevier B V

U2 - 10.1016/j.brainres.2010.08.036

DO - 10.1016/j.brainres.2010.08.036

M3 - Literature review

SN - 1873-2747

VL - 1364

SP - 153

EP - 163

JO - Brain Research

JF - Brain Research

ER -