Abstract:
:Dehydroepiandrosterone sulfate (DHEAS) dose-dependently inhibited [3H]norepinephrine (NE) secretion and the corresponding [Ca2+]i rise induced by the nicotinic receptor agonist 1,1-dimethyl-4-phenylpoperazimium (DMPP) in bovine chromaffin cells. DHEAS at 10 microM, the physiological concentration in human serum, significantly inhibited both the release of [3H]NE and the rise of [Ca2+]i induced by DMPP in chromaffin cells. DHEAS also inhibited the [3H]NE release induced by the Na+ channel activator veratridine. However, DHEAS did not affect either the [3H]NE release, or the corresponding [Ca2+]i rise induced by high K+. Moreover, DHEAS suppressed the [Na+]i rise induced by either DMPP or high K+ as monitored by the fluorescence 340/380 ratio of SBFI loaded chromaffin cells. Our results suggest that the inhibitory effects of DHEAS on secretion mainly occur at nicotinic receptors as well as at the voltage-dependent Na+ channels.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Liu PS,Lin MK,Hsieh HLdoi
10.1016/0304-3940(96)12350-8subject
Has Abstractpub_date
1996-02-09 00:00:00pages
181-4issue
3eissn
0304-3940issn
1872-7972pii
0304394096123508journal_volume
204pub_type
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journal_title:Neuroscience letters
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journal_title:Neuroscience letters
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journal_title:Neuroscience letters
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journal_title:Neuroscience letters
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journal_title:Neuroscience letters
pub_type: 杂志文章
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