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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
50
pubmed:dateCreated
2000-1-13
pubmed:abstractText
In excitable cells, oscillations in intracellular free calcium concentrations ([Ca(2+)](i)) can arise from action-potential-driven Ca(2+) influx, and such signals can have either a localized or global form, depending on the coupling of voltage-gated Ca(2+) influx to intracellular Ca(2+) release pathway. Here we show that rat pituitary somatotrophs generate spontaneous [Ca(2+)](i) oscillations, which rise from fluctuations in the influx of external Ca(2+) and propagate within the cytoplasm and nucleus. The addition of caffeine and ryanodine, modulators of ryanodine-receptor channels, and the depletion of intracellular Ca(2+) stores by thapsigargin and ionomycin did not affect the global nature of spontaneous [Ca(2+)](i) signals. Bay K 8644, an L-type Ca(2+) channel agonist, initiated [Ca(2+)](i) signaling in quiescent cells, increased the amplitude of [Ca(2+)](i) spikes in spontaneously active cells, and stimulated growth hormone secretion in perifused pituitary cells. Nifedipine, a blocker of L-type Ca(2+) channels, decreased the amplitude of spikes and basal growth hormone secretion, whereas Ni(2+), a blocker of T-type Ca(2+) channels, abolished spontaneous [Ca(2+)](i) oscillations. Spiking was also abolished by the removal of extracellular Na(+) and by the addition of 10 mM Ca(2+), Mg(2+), or Sr(2+), the blockers of cyclic nucleotide-gated channels. Reverse transcriptase-polymerase chain reaction and Southern blot analyses indicated the expression of mRNAs for these channels in mixed pituitary cells and purified somatotrophs. Growth hormone-releasing hormone, an agonist that stimulated cAMP and cGMP productions in a dose-dependent manner, initiated spiking in quiescent cells and increased the frequency of spiking in spontaneously active cells. These results indicate that in somatotrophs a cyclic nucleotide-controlled plasma membrane Ca(2+) oscillator is capable of generating global Ca(2+) signals spontaneously and in response to agonist stimulation. The Ca(2+)-signaling activity of this oscillator is dependent on voltage-gated Ca(2+) influx but not on Ca(2+) release from intracellular stores.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
274
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
35693-702
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:10585449-3-Pyridinecarboxylic acid..., pubmed-meshheading:10585449-Action Potentials, pubmed-meshheading:10585449-Animals, pubmed-meshheading:10585449-Calcium, pubmed-meshheading:10585449-Cell Membrane, pubmed-meshheading:10585449-Cells, Cultured, pubmed-meshheading:10585449-Cyclic AMP, pubmed-meshheading:10585449-Cyclic GMP, pubmed-meshheading:10585449-Cyclic Nucleotide-Gated Cation Channels, pubmed-meshheading:10585449-Endothelin-1, pubmed-meshheading:10585449-Female, pubmed-meshheading:10585449-Gonadotropin-Releasing Hormone, pubmed-meshheading:10585449-Ion Channels, pubmed-meshheading:10585449-Ionomycin, pubmed-meshheading:10585449-Kinetics, pubmed-meshheading:10585449-Nifedipine, pubmed-meshheading:10585449-Pituitary Gland, Anterior, pubmed-meshheading:10585449-Rats, pubmed-meshheading:10585449-Rats, Sprague-Dawley, pubmed-meshheading:10585449-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:10585449-Signal Transduction, pubmed-meshheading:10585449-Thyrotropin-Releasing Hormone
pubmed:year
1999
pubmed:articleTitle
Characterization of a plasma membrane calcium oscillator in rat pituitary somatotrophs.
pubmed:affiliation
Endocrinology and Reproduction Research Branch, NICHD, National Institutes of Health, Bethesda, Maryland 20892-4510, USA.
pubmed:publicationType
Journal Article