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

• Published in: Brain research Vol. 903; no. 1; pp. 62 - 65
• Main Authors: Tomé, Angelo R., Izaguirre, Victor, Rosário, Luı́s M., Ceña, Valentı́n, González-Garcı́a, Carmen
• Format: Journal Article
• Language: English
• Published: London Elsevier B.V 08-06-2001; Amsterdam Elsevier; New York, NY
• Subjects: Adrenals. Interrenals; Adrenomedullary hormones. Regulation; Animals; Biological and medical sciences; Catecholamine secretion; Catecholamines - metabolism; Cattle; Chromaffin Cells - cytology; Chromaffin Cells - metabolism; Chromaffin Cells - physiology; Currents; Dose-Response Relationship, Drug; Fundamental and applied biological sciences. Psychology; Membrane Potentials - drug effects; Membrane Potentials - physiology; Naloxone - pharmacology; Narcotic Antagonists - pharmacology; Nicotine - pharmacology; Nicotinic Agonists - pharmacology; Nicotinic receptor; Opioid Peptides - antagonists & inhibitors; Opioids; Patch-clamp; Patch-Clamp Techniques; Receptors, Nicotinic - physiology; Vertebrates: endocrinology; Catecholamine secretion; Currents; Patch-clamp; Neurotransmitters, modulators, transporters, and receptors; Nicotinic receptor; Opioids; Endocrine gland; Secretion; Adrenal medulla; Electrophysiology; Ox; Patch clamp method; Ionic current; Catecholamine; Chromaffin cell; Cholinergic receptor; Vertebrata; Mammalia; Naloxone; Artiodactyla; Ungulata
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/S0006-8993(01)02388-5

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 (IC
50=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.