Linked Life Data

19641296

Source:http://linkedlifedata.com/resource/pubmed/id/19641296

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2009-10-15
pubmed:abstractText
Melatonin has been implicated in the control of the reproductive system, and the modulatory actions of melatonin on gonadotropin-releasing hormone (GnRH) neurons have been assumed to be indirectly mediated through afferent neurons. However, our previous studies demonstrate sexually dimorphic modulation of A-type gamma-aminobutyric acid (GABA) receptor (GABA(A)R) currents by melatonin in adult rat GnRH neurons and a preferential expression of melatonin 1a receptor (MT1) in male GnRH neurons. Using immortalized GnRH neurons (GT1-7 cells), the present study investigated the mechanism by which the expression of melatonin receptors is regulated in GnRH neurons. Like endogenous GnRH neurons, GT1-7 cells express both GnRH and GnRH receptor mRNAs, indicating that the cells have a self-stimulatory system. A 2-iodomelatonin binding assay and RT-PCR analysis demonstrated that the cells expressed neither MT1 nor MT2. However, treatment of GT1-7 cells with the GnRH antagonist cetrorelix significantly increased 2-iodomelatonin binding and induced a time- and concentration-dependent MT1 mRNA expression. The GABA(A)R currents were then measured using a perforated patch-clamp technique to examine whether the treatment with cetrorelix changed the responses to melatonin. Melatonin augmented the GABA(A)R currents in GT1-7 cells treated with 1 muM cetrorelix for 24 h, while melatonin decreased the currents in the cells not treated with cetrorelix, probably via receptor-independent processes. The present results suggest that GnRH downregulates the expression of MT1 via an autocrine-paracrine mechanism in GT1-7 cells, and modifies the melatonin-induced modulation of GABA(A)R currents. These findings may provide one possible mechanism for the sexually dimorphic responses to melatonin in adult rat GnRH neurons.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1423-0194
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
90
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
251-9
pubmed:meshHeading
pubmed-meshheading:19641296-Animals, pubmed-meshheading:19641296-Cell Line, pubmed-meshheading:19641296-Cell Line, Tumor, pubmed-meshheading:19641296-Central Nervous System Depressants, pubmed-meshheading:19641296-Dose-Response Relationship, Drug, pubmed-meshheading:19641296-Gonadotropin-Releasing Hormone, pubmed-meshheading:19641296-Hormone Antagonists, pubmed-meshheading:19641296-Humans, pubmed-meshheading:19641296-Melatonin, pubmed-meshheading:19641296-Membrane Potentials, pubmed-meshheading:19641296-Mice, pubmed-meshheading:19641296-NIH 3T3 Cells, pubmed-meshheading:19641296-Neurons, pubmed-meshheading:19641296-RNA, Messenger, pubmed-meshheading:19641296-Receptor, Melatonin, MT1, pubmed-meshheading:19641296-Receptor, Melatonin, MT2, pubmed-meshheading:19641296-Receptors, GABA-A, pubmed-meshheading:19641296-Receptors, LHRH, pubmed-meshheading:19641296-Time Factors
pubmed:year
2009
pubmed:articleTitle
Cetrorelix, a gonadotropin-releasing hormone antagonist, induces the expression of melatonin receptor 1a in the gonadotropin-releasing hormone neuronal cell line GT1-7.
pubmed:affiliation
Department of Physiology, Nippon Medical School, Tokyo, Japan. hirotaka@nms.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't