Study On The Puberty Regulatory Mechanisms Of Central Nervous System In Mice

Puberty reflects the physiological processes that guide the awakening of the adultneuroendocrine reproductive axis in mammalians. Puberty is marked by the increase inhypothalamic gonadotropin-releasing hormone (GnRH) secretion. It is not known whatstimulates the initial increase in GnRH secretion at puberty, or alternatively, whatinhibits GnRH secretion until the onset of puberty. RFRP-3is the only hypothalamicneuropeptide yet indicated that has capacity to restrain the HPG axis. RFRP-3plays acrucial role in the modulation of HPG axis function as a critical negative modulatorbetween different species in spite of few specialized study. Thus, this research is amiedat analyzing puberty regulatory mechanisms of central nervous system in mice:①bydetecting t developmental changes in plasma luteinizing hormone (LH) release and inhypothalamic related genes mRNA expression, to speculate nervous factor whichinvolved in onset of puberty;②d etected theeffects of neuropeptide on hypothalamicrelated genes expression and plasma LH secretion. The results are as follows:①During the pubertal development process: Plasma LH concentrations didn’tchange significantly before prepuberty, and increased at vaginal opening day;Kiss1/GPR54mRNA expression levels continued to increase until onset of puberty infemale mice, and declined at mature period; Level of RFRP mRNA and GPR147mRNAincreased from days28and32, respectively, and both peaking at days32. However,expression levels of both molecules fell at vaginal opening day and were significantlylower than their peak values, as well as slightly increased at mature period; Neither Tac2mRNA nor PAYN mRNA had significantly changes with development.②It was confirmed that RFRP-3had significantly suppressed plasma LH levels inprepubertal female mice, which involves a E2-dependent mechanism, whereas RF9, thereceptor antagonist of RFRP, significantly increased plasma LH levels in intactprepubertal female mice; Excepting increased GnRH mRNA expression, RFRP-3significantly the genes mRNA level of KNDy neurons; Neither RFRP-3nor estrogenhad significant role on ERα mRNA expression in hypothalamus. These resultssuggested that more research need to clarify whether E2negative feedback involves inRFRP-3inhibitory on reproductive function in mammalians.③Detected the effects of arcuate nucleus KNDy neurons on pubertaldevelopment in female mice: kisspeptin significantly promoted plasma LH secretion, whereas Kp234, the receptor antagonist of kisspeptin, had nonsignificantly effects onLH secretion; NKB agonist senktide, inhibited LH secretion, whlie the effect is notsignificant; In addition, U50488, dynorphin receptor agonists, significantly suppressedserum LH levels.