Melatonin inhibits GnRH-induced Ca2+ mobilization and influx through voltage-regulated channels
Language English Country Switzerland Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
9500667
DOI
10.1159/000109139
Knihovny.cz E-resources
- MeSH
- Pituitary Gland, Anterior cytology MeSH
- Ion Channel Gating MeSH
- Gonadotropin-Releasing Hormone antagonists & inhibitors pharmacology MeSH
- Rats MeSH
- Cells, Cultured MeSH
- Melatonin pharmacology MeSH
- Animals, Newborn MeSH
- Rats, Wistar MeSH
- Calcium metabolism MeSH
- Calcium Channels drug effects metabolism MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Gonadotropin-Releasing Hormone MeSH
- Melatonin MeSH
- Calcium MeSH
- Calcium Channels MeSH
In neonatal rat gonadotrophs, melatonin acts through the high-affinity membrane-bound receptors to inhibit GnRH-induced [Ca2+]i increase. GnRH increases [Ca2+]i primarily by mobilization from the inositol trisphosphate-sensitive pool followed by Ca2+ influx through the voltage-sensitive channels. Melatonin inhibits the GnRH-induced [Ca2+]i increase. When added after the GnRH-induced spike, melatonin decreases [Ca2+]i in 52% of the gonadotrophs. The effect of melatonin is dependent on extracellular Ca2+ and may be mimicked by Ca2+-free medium or verapamil. When added before GnRH, melatonin inhibits the [Ca2+]i spike. This effect of melatonin is independent of extracellular Ca2+ as it persists in Ca2+-free medium. These findings indicate that melatonin blocks Ca2+ mobilization as well as Ca2+ influx in the gonadotrophs.
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