| Literature DB >> 27343174 |
Yuki Arai1,2, Hirotaka Ishii3, Makito Kobayashi2, Hitoshi Ozawa1.
Abstract
GnRH neurons form a final common pathway for the central regulation of reproduction. Although the involvement of acetylcholine in GnRH secretion has been reported, direct effects of acetylcholine and expression profiles of acetylcholine receptors (AChRs) still remain to be studied. Using immortalized GnRH neurons (GT1-7 cells), we analyzed molecular expression and functionality of AChRs. Expression of the mRNAs were identified in the order α7 > β2 = β1 ≧ α4 ≧ α5 = β4 = δ > α3 for nicotinic acetylcholine receptor (nAChR) subunits and m4 > m2 for muscarinic acetylcholine receptor (mAChR) subtypes. Furthermore, this study revealed that α7 nAChRs contributed to Ca2+ influx and GnRH release and that m2 and m4 mAChRs inhibited forskolin-induced cAMP production and isobutylmethylxanthine-induced GnRH secretion. These findings demonstrate the molecular profiles of AChRs, which directly contribute to GnRH secretion in GT1-7 cells, and provide one possible regulatory action of acetylcholine in GnRH neurons.Entities:
Keywords: Acetylcholine; Acetylcholine receptors; GT1-7; GnRH neurons; Gonadotropin-releasing hormone
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Year: 2016 PMID: 27343174 DOI: 10.1007/s12576-016-0464-1
Source DB: PubMed Journal: J Physiol Sci ISSN: 1880-6546 Impact factor: 2.781