Naloxone inhibits nicotine-induced receptor current and catecholamine secretion in bovine chromaffin cells

Angelo R. Tomé, Victor Izaguirre, Luís M. Rosário, Valentín Cea, Carmen González-García

Research output: Contribution to journalArticle

23 Scopus citations

Abstract

Nicotine-induced catecholamine (CA) secretion and inward ionic currents were inhibited by the opioid antagonist naloxone in cultured bovine chromaffin cells. Naloxone inhibited nicotine-induced CA secretion, as detected by an on-line real-time electrochemical technique, in a dose-dependent manner (IC50=29 μM). In voltage-clamped chromaffin cells, nicotine (10 μM) evoked an average peak inward current of -146 pA that was inhibited by low concentrations of naloxone (42% at 0.1 μM). The antagonist also inhibited total charge influx associated with nicotinic receptor activation (53% at 0.1 μM). This provides strong evidence that naloxone modulation of nicotine-induced CA secretion does not involve opioid receptors but results from the direct interaction with the nicotinic receptor itself, which might also be the case for other related opioid compounds. © 2001 Elsevier Science B.V. All rights reserved.
Original languageAmerican English
Pages (from-to)62-65
Number of pages4
JournalBrain Research
DOIs
StatePublished - 8 Jun 2001
Externally publishedYes

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