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The Effect of Oestradiol and Progesterone on Hypoglycaemic Stress‐Induced Suppression of Pulsatile Luteinizing Hormone Release and on Corticotropin‐Releasing Hormone mRNA Expression in the Rat
Author(s) -
Li X. F.,
Mitchell J. C.,
Wood S.,
Coen C. W.,
Lightman S. L.,
O'Byrne K. T.
Publication year - 2003
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.1365-2826.2003.01014.x
Subject(s) - medicine , endocrinology , luteinizing hormone , corticosterone , corticotropin releasing hormone , hypothalamus , ovariectomized rat , pulsatile flow , hormone , chemistry , biology
Corticotropin‐releasing hormone (CRH) is implicated in the suppression of pulsatile luteinizing hormone (LH) secretion by a variety of stressful stimuli; 17β‐oestradiol (E 2 ) has been shown to modulate this inhibitory response. The present study in ovariectomized (OVX) rats was designed to investigate the effect of E 2 and progesterone (P 4 ) on hypoglycaemic stress‐induced changes in pulsatile LH secretion and on the associated changes in both central and peripheral components of the hypothalamic‐pituitary‐adrenal axis. E 2 enhanced the hypoglycaemic stress‐induced suppression of LH pulses; P 4 in addition to E 2 further potentiated the inhibitory response. The rise in plasma corticosterone following insulin‐induced hypoglycaemia (IIH) was highest in the E 2 + P 4 group. Nevertheless, when such levels were achieved by administration of corticosterone, the occurrence of LH pulses was completely unaffected, irrespective of ovarian steroid milieu. E 2 and E 2 + P 4 up‐regulated basal CRH mRNA expression in the paraventricular nucleus (PVN) as measured by in situ hybridization; this signal was also increased in the medial preoptic nucleus (MPN) following E 2 . IIH resulted in a rise in CRH mRNA in the PVN, but not in the MPN; this rise may reflect a more significant role for the PVN in the present context. Changes in neuropeptide mRNA expression may signal changes in neuronal activity; nevertheless, the profound differences in LH pulse suppression in OVX, E 2 and E 2 + P 4 rats following IIH were not reflected in the concurrent changes in CRH mRNA in the PVN. The results suggest that while corticosterone has no acute effect on LH pulses in the rat, the up‐regulation by ovarian steroids of basal CRH mRNA in the PVN and/or MPN may contribute to the central regulation of these pulses in response to stress.