Journal of neuroendocrinology
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J. Neuroendocrinol. · Oct 1998
Role of endogenous opiates in glucoprivic inhibition of the luteinizing hormone surge and fos expression by preoptic gonadotropin-releasing hormone neurones in ovariectomized steroid-primed female rats.
In female mammals, the preovulatory luteinizing hormone (LH) 'surge' elicits ovulation and the subsequent transformation of Graafian follicles into corpora lutea, and is thus a critical component of successful reproduction. In light of evidence that this surge is impaired as a consequence of caloric restriction, the following experiments utilized pharmacological strategies to determine whether glucose substrate homeostasis influences the magnitude and/or duration of this pivotal hormonal event. Groups of oestrogen-and progesterone-primed ovariectomized (OVX) rats were injected intravenously (i.v.) with the glucose antimetabolite, 2-deoxy-D-glucose (2DG: 100 or 400 mg/kg), or the vehicle, saline, prior to onset of the expected LH surge. ⋯ Animals pretreated with 2DG i.c.v showed a significant decrease in mean numbers of GnRH neurones exhibiting Fos-ir, whereas coadministration of 2DG and NALT resulted in numbers of double-labelled neurones that were similar to those detected in the non-drug-treated controls. These studies show that magnitude of the LH surge is decreased by glucose substrate imbalance, and that regulatory effects of this metabolic challenge on the reproductive neuroendocrine axis is correlated with alterations in the transcriptional activation of preoptic GnRH neurones by gonadal steroid positive feedback. The present results also support a role for central opiatergic neurotransmission in glucoprivic regulation of cyclic LH secretion in this animal model.