2000
DOI: 10.1016/s0006-8993(00)02492-6
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Inhibition by neuroprotective drug NS-7 of nicotine-induced 22Na+ influx, 45Ca2+ influx and catecholamine secretion in adrenal chromaffin cells

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Cited by 4 publications
(2 citation statements)
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“…Nicotine can cause intracellular Na ϩ influx via cation-channel-coupled nicotinic acetylcholine receptors during depolarization of the cell membrane, and as a result can cause Ca 2ϩ influx via voltage dependent Ca 2ϩ channels. 12,13) However, in the present study SEA0400 had no effect on nicotine-induced convulsions. Taken together, our data suggest that the mechanism of PTZ-induced expression and action of convulsion is very complex, but Ca 2ϩ influx via NCX seem to be important.…”
contrasting
confidence: 77%
“…Nicotine can cause intracellular Na ϩ influx via cation-channel-coupled nicotinic acetylcholine receptors during depolarization of the cell membrane, and as a result can cause Ca 2ϩ influx via voltage dependent Ca 2ϩ channels. 12,13) However, in the present study SEA0400 had no effect on nicotine-induced convulsions. Taken together, our data suggest that the mechanism of PTZ-induced expression and action of convulsion is very complex, but Ca 2ϩ influx via NCX seem to be important.…”
contrasting
confidence: 77%
“…Secretion and transcription of catecholamines upon nicotinic cholinergic activation are triggered by sodium entry followed by a transient calcium influx that is mediated by voltage gated calcium channels (VGCCs; [194]). Nicotine also induces a dose-dependent increase in the intracellular calcium concentration [Ca ++ ] i via increasing calcium influx from extracellular space, and activating inositol(1,4,5)-trisphosphate (IP3) receptor-coupled intracellular calcium reserves.…”
Section: Signaling Pathways Involved In Catecholamine Synthesis and Rmentioning
confidence: 99%