This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.To understand the mechanism of LHRH pulse generation and the mechanism of steroid action on LHRH neurons.Pulsatile release of LHRH from the hypothalamus is essential for normal reproductive function, yet the mechanism of LHRH pulse generation is unclear. We cultured LHRH neurons originating from the olfactory pit/placode region and characterized the cellular mechanism of LHRH pulse generation. The periodicity of peptide release and bursting activity of LHRH neurons were much slower than mouse LHRH neurons, although many characteristics in monkey LHRH neurons are similar to those described for mice. We also found that LHRH neurons respond to estrogen with a short latency (within several minutes), stimulating the frequency of firing activity and intracellular calcium oscillations, and LHRH release. This rapid action of estrogen occurs at the cell membrane and is not blocked by nuclear estrogen receptor blockers indicating that there is a mechanism yet to be described. Because recently we found that LHRH neurons expressed the 7-transmembrane receptor, GPR30, and the rapid effect of estrogen can be blocked by G-protein interference, we hypothesize that GPR30 is, in part, involved in the rapid action of estrogen. These preliminary findings are important for the development of contraceptive tools and treatment of infertility. This research used WNPRC Animal Services and Assay Services.
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