Sodium-dependent effects of melatonin on membrane potential of neonatal rat pituitary cells
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články
- MeSH
- buněčná membrána účinky léků fyziologie MeSH
- faktory virulence rodu Bordetella farmakologie MeSH
- fluorescenční barviva MeSH
- hormon uvolňující gonadotropiny farmakologie MeSH
- hypofýza fyziologie ultrastruktura MeSH
- inbrední kmeny potkanů MeSH
- krysa rodu Rattus MeSH
- melatonin farmakologie MeSH
- melatoninové receptory MeSH
- membránové potenciály účinky léků MeSH
- novorozená zvířata fyziologie MeSH
- pertusový toxin MeSH
- receptory neurotransmiterů fyziologie MeSH
- sodík farmakologie MeSH
- stárnutí MeSH
- vápník metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- faktory virulence rodu Bordetella MeSH
- fluorescenční barviva MeSH
- hormon uvolňující gonadotropiny MeSH
- melatonin MeSH
- melatoninové receptory MeSH
- pertusový toxin MeSH
- receptory neurotransmiterů MeSH
- sodík MeSH
- vápník MeSH
Melatonin inhibits GnRH-stimulated release of LH from neonatal rat pituitary cells, probably by inhibiting GnRH-induced elevation of intracellular Ca2+. This effect of melatonin seems to involve inhibition of Ca2+ influx through voltage-sensitive channels. Accordingly, it is possible that melatonin could act by hyperpolarizing pituitary cells, which would close these channels. This issue was addressed here by determining if melatonin influences membrane potential. Membrane potential and intracellular Ca2+ were studied in neonatal rat pituitary cells in suspension, using bis-oxonol and Fluo-3 as fluorescent indicators, respectively. It was found that treatment with melatonin alone causes membrane hyperpolarization and that it has a repolarizing effect after GnRH-induced membrane depolarization. This effect on membrane potential appears to be mediated by high affinity melatonin receptors and a pertussis toxin-sensitive Na(+)-dependent mechanism; it is not dependent upon Ca2+, Cl-, or bicarbonate. This may be the molecular basis of action of melatonin in other tissues with high affinity melatonin receptors.
Citace poskytuje Crossref.org
Ion Channels of Pituitary Gonadotrophs and Their Roles in Signaling and Secretion