INDUCTION OF GALANIN GENE EXPRESSION IN GnRH NEURONS WITH PUBERTY IN THE FEMALE RAT

Abstract

Puberty is characterized by increasing plasma levels of gonadotropins, which are thought to be mediated by an increase in the pulsatile secretion of gonadotropin releasing hormone (GnRH) from the hypothalamus. Although hypothalamic content of GnRH increases with puberty, cellular levels of its precursor mRNA remain stable indicating that overall biosynthetic demand for GnRH does not change as a function of puberty. While alterations in afferent activity at the GnRH neuron have been suggested as a mechanism for modulating the release of GnRH at puberty, changes intrinsic to the GnRH neuron itself also remain as plausible governing events. Galanin is a recently described gut-brain peptide that is colocalized with GnRH in hypothalamic neurons where it is thought to play a role in the orchestration of gonadotropin release. We tested the hypothesis that the expression of the galanin gene in GnRH neurons is altered during puberty in female rats. To accomplish this, we sacrificed groups of prepubertal (25 day; n=5) and adult (70 day; n=6) female rats and utilized double in situ hybridization and image analysis to estimate and compare between groups the number of GnRH mRNA expressing neurons that coexpress galanin mRNA. While the number of GnRH neurons identified was not different between groups (prepubertal 27 ± 4 vs. adult 30 ± 3) the number of GnRH neurons coexpressing galanin mRNA was greatly increased after puberty (prepubertal 6 ± 3% vs. adult 45 ± 9%; p<0.006).

Conclusion: The apparent increase in galanin biosynthesis in GnRH neurons may subserve the augmentation of pulsatile GnRH release driving the onset of puberty in the rat.

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