Involvement of an autoregulatory mechanism for the regulation of gonadotropin-releasing hormone (GnRH) gene expression in neurons in the rat preoptic area.

To verify the hypothesis that GnRH neurons can influence each other, we have studied the effects of GnRH, a potent GnRH agonist (Des-Gly10, D-Ala6-proethylamide9)-GnRH and a GnRH antagonist Antide on GnRH gene expression in the male rat preoptic area (POA). Hypophysectomized rats received into the left lateral brain ventricle either the vehicle or each of the peptides. GnRH mRNA levels in neurons in POA were evaluated by quantitative in situ hybridization using a 35S-labelled 48-base oligonucleotide. In hypophysectomized animals, a 18% decrease in the number of silver grain overlying GnRH neurons was observed as compared to intact animals. In hypophysectomized animals neither GnRH nor the GnRH agonist modified GnRH mRNA levels. On the other hand, the administration of Antide induced a 34% increase in the levels of GnRH mRNA. These results suggest that GnRH exerts a negative regulation of the GnRH gene expression in neurons in the POA probably via GnRH receptors.