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Effect of Corticotropin‐Releasing Hormone Antagonist on Oestrogen‐Dependent Glucoprivic Suppression of Luteinizing Hormone Secretion in Female Rats
Author(s) -
Shinji Tsukahara,
Hiroko Tsukamura,
Douglas L. Foster,
Keiichiro Maeda
Publication year - 1999
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1046/j.1365-2826.1999.00312.x
Subject(s) - endocrinology , medicine , pulsatile flow , ovariectomized rat , luteinizing hormone , cannula , antagonist , chemistry , hormone , median eminence , corticotropin releasing hormone , receptor , surgery
Pharmacological reduction of glucose availability with 2‐deoxyglucose (2DG) suppresses pulsatile luteinizing hormone (LH) secretion in rats and growth‐retarded lambs. Gonadal steroids enhance the glucoprivic suppression of LH secretion in rats. The present study determined if corticotropin‐releasing hormone (CRH) plays a role in mediating oestrogen‐dependent and ‐independent glucoprivic suppression of LH secretion. The study was conducted in ovariectomized (OVX) rats some of which received Silastic implants containing oestradiol‐17 β (OE 2 ) dissolved in peanut oil at 20 μg/ml to produce a physiological plasma level of OE 2 (30 pg/ml). Seven days after ovariectomy, the rats were stereotaxically implanted with a guide cannula into the third cerebral ventricle. Seven days later, blood samples were collected through an indwelling atrial cannula every 6 min for 3 h for LH pulse determination. After the first hour of blood sampling, a CRH antagonist, [ d ‐Phe 12 , Nle 21,38 ]hCRF‐(21–41), or vehicle was injected into the third cerebral ventricle through the implanted cannula before 2DG administration through the indwelling atrial cannula. Pulsatile LH secretion was suppressed by 2DG (200 mg/kg b.w.) in the vehicle‐treated rats bearing OE 2 implants. The CRH antagonist (5.65 nmol) blocked the suppressive effect of 2DG on pulsatile LH secretion in the OE 2 ‐treated OVX animals. On the other hand, in the absence of oestrogen, the effect of a twice greater dose of 2DG (400 mg/kg b.w.) was not blocked by five times greater amount of CRH antagonist (28.3 nmol). These results suggest the mechanisms mediating glucoprivic suppression of LH secretion involve two components: one is oestrogen‐dependent and the other oestrogen‐independent. CRH may be involved in the oestrogen‐dependent component of glucoprivic suppression of LH secretion but not the oestrogen‐independent one.