Abstract:
:In NG 108-15 clonal cells, extracellular application of micromolar concentrations of serotonin [5-hydroxytryptamine (5-HT)] and substance P induces the opening of a cation permeability monitored by the influx of [14C]-guanidinium. The serotoninergic component of this cation permeability is linked to 5-HT3 receptor activation, whereas the substance P component probably involves an "N-terminal-dependent substance P receptor." In this study, [14C]guanidinium influx triggered by 1 microM 5-HT plus 10 microM substance P was shown to be insensitive to tetrodotoxin, verapamil, diltiazem, nimodipine, and omega-conotoxin, as expected from a process independent of voltage-sensitive sodium and calcium channels. In contrast, [14C]guanidinium influx was inhibited by millimolar concentrations of extracellular calcium and by the chelation of intracellular calcium by bis-O-aminophenoxyethanetetraacetic acid. The inhibition by extracellular calcium apparently involved a competition between the divalent cation and [14C]guanidinium for the same channel. When NG 108-15 cells were exposed to X537A, an ionophore that specifically induces release of calcium from intracellular stores, [14C]guanidinium uptake was markedly increased even in the absence of 5-HT and/or substance P. Conversely, [14C]guanidinium influx due to the latter substances could be reversibly and dose-dependently blocked by various drugs that possess calmodulin-antagonizing properties. These results strongly suggest that the cation permeability opened by 5-HT and substance P in NG 108-15 cells involves a calcium/calmodulin-dependent process.(ABSTRACT TRUNCATED AT 250 WORDS)
journal_name
J Neurochemjournal_title
Journal of neurochemistryauthors
Riad M,Hamon M,Emerit MBdoi
10.1046/j.1471-4159.1994.62062224.xsubject
Has Abstractpub_date
1994-06-01 00:00:00pages
2224-32issue
6eissn
0022-3042issn
1471-4159journal_volume
62pub_type
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
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pub_type: 杂志文章
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
doi:10.1111/j.1471-4159.1990.tb01228.x
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journal_title:Journal of neurochemistry
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pub_type: 杂志文章
doi:10.1111/j.1471-4159.1992.tb08319.x
更新日期:1992-09-01 00:00:00
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
doi:10.1046/j.1471-4159.1999.0720585.x
更新日期:1999-02-01 00:00:00
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doi:10.1111/j.1471-4159.1988.tb10599.x
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pub_type: 杂志文章
doi:10.1111/j.1471-4159.1993.tb09806.x
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
doi:10.1111/j.1471-4159.1991.tb08291.x
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
doi:10.1111/j.1471-4159.1991.tb02586.x
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
doi:10.1046/j.1471-4159.1994.63031003.x
更新日期:1994-09-01 00:00:00
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
doi:10.1111/j.1471-4159.1984.tb06686.x
更新日期:1984-07-01 00:00:00