Effect of corticotropin-releasing hormone antagonist on oestrogen-dependent glucoprivic suppression of luteinizing hormone secretion in female rats.
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-17beta (OE2) dissolved in peanut oil at 20 microg/ml to produce a physiological plasma level of OE2 (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-Phe12, Nle21,38]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 OE2 implants. The CRH antagonist (5.65 nmol) blocked the suppressive effect of 2DG on pulsatile LH secretion in the OE2-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.
Tsukahara
S
S
School of Agricultural Sciences, Nagoya University, Chikusa, Japan.
Tsukamura
H
H
Foster
D L
DL
Maeda
K I
KI
D000818:Animals; D000963:Antimetabolites / Q000494:pharmacology; D001923:Brain Chemistry / Q000187:drug effects*; D003346:Corticotropin-Releasing Hormone / Q000037:antagonists & inhibitors*; D003847:Deoxyglucose / Q000494:pharmacology; D004967:Estrogens / Q000494:pharmacology*; D005260:Female; D005947:Glucose / Q000378:metabolism*; D007276:Injections, Intraventricular; D007986:Luteinizing Hormone / Q000378:metabolism*; D009490:Neurosecretory Systems / Q000187:drug effects / Q000502:physiology; D010052:Ovariectomy; D011673:Pulsatile Flow; D051381:Rats; D017208:Rats, Wistar
D000963:Antimetabolites; D004967:Estrogens; D007986:Luteinizing Hormone; D003346:Corticotropin-Releasing Hormone; D003847:Deoxyglucose; D005947:Glucose