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.
|Number of pages||4|
|State||Published - 8 Jun 2001|
Bibliographical noteFunding Information:
This work has been supported in part by grants SAF96-0169 and 1FD97-0500 from CICYT to V.C.; PRAXIS 2/2.1/SAU/1179/95 from Fundação para a Ciência e Tecnologia (FCT) to L.M.R. and SAF98-0140 from CICYT to C.G.G.
- Catecholamine secretion
- Nicotinic receptor