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Melatonin receptor expression exhibits profound developmental changes through poorly understood mechanisms. In mammals, a current model suggests that pubertal reactivation of gonadotrophin-releasing hormone (GnRH) secretion down-regulates MT1 melatonin receptors in pituitary gonadotroph cells, via the induction of early growth response factor-1 (EGR-1). Here we have examined this model by testing the hypotheses that inhibition of  Mt1  expression by GnRH occurs directly in gonadotroph cells, can be reversed in adulthood by blockade of GnRH receptors, and requires EGR-1. We first confirmed the endogenous expression of  Mt1  mRNA in the αT3-1 gonadotroph cell line. Stimulation of these cells with a GnRH agonist resulted in a rapid increase of  Egr-1  mRNA expression, which peaked after 30–60 minutes, and a more prolonged elevation of nuclear EGR-1 immunoreactivity. Moreover, the GnRH agonist significantly decreased  Mt1  mRNA. We then treated adult male rats with the GnRH antagonist cetrorelix or saline. After 4 weeks of daily injections, cetrorelix significantly reduced serum LH concentration and testis weight, with histological analysis confirming absence of spermatogenesis. Despite the successful inhibition of GnRH signalling, pituitary  Mt1  expression was unchanged. Next we studied the proximal region of the rat  Mt1  promoter. Consistent with previous work, over-expression of the transcription factor PITX-1 increased  Mt1 -luciferase reporter activity; this effect was dependent on the presence of consensus PITX-1 promoter binding regions. Over-expression of EGR-1 inhibited PITX-1-stimulated activity, even following mutation of the consensus EGR-1 binding site. Finally, we studied  Egr1   −/−  mice and observed no difference in pituitary  Mt1  expression between  Egr1   −/−  and wild-type litter mates. This work demonstrates that GnRH receptor activation directly down-regulates  Mt1  expression in gonadotroph cells. However, pituitary  Mt1  expression in adults is unaltered by blockade of GnRH signalling or absence of EGR-1. Our data therefore suggest that melatonin receptor regulation by GnRH is not reversible in adulthood and doesn't require EGR-1.

plos one

Regulation of Pituitary MT1 Melatonin Receptor Expression by Gonadotrophin-Releasing Hormone (GnRH) and Early Growth Response Factor-1 (Egr-1): In Vivo and In Vitro Studies