Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Bupropion is a nicotinic antagonist
Autore:
Slemmer, JE; Martin, BR; Damaj, MI;
Indirizzi:
Virginia Commonwealth Univ, Med Coll Virginia, Dept Pharmacol & Toxicol, Richmond, VA 23298 USA Virginia Commonwealth Univ Richmond VA USA 23298 , Richmond, VA 23298 USA
Titolo Testata:
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
fascicolo: 1, volume: 295, anno: 2000,
pagine: 321 - 327
SICI:
0022-3565(200010)295:1<321:BIANA>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
SMOKING CESSATION; PHARMACOLOGICAL CHARACTERIZATION; MICE; METABOLITES; INHIBITION; MECHANISM; MORPHINE; BINDING; BRAIN; RATS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
27
Recensione:
Indirizzi per estratti:
Indirizzo: Damaj, MI Virginia Commonwealth Univ, Med Coll Virginia, Dept Pharmacol & Toxicol, Richmond, VA 23298 USA Virginia Commonwealth Univ Richmond VA USA23298 , VA 23298 USA
Citazione:
J.E. Slemmer et al., "Bupropion is a nicotinic antagonist", J PHARM EXP, 295(1), 2000, pp. 321-327

Abstract

Neuronal nicotinic receptors are ligand-gated ion channels of the central and peripheral central nervous system that regulate synaptic activity from both pre- and postsynaptic sites. The present study establishes the acute interaction of bupropion, an antidepressant agent that is also effective in nicotine dependence, with nicotine and nicotinic receptors using different in vivo and in vitro tests. Bupropion was found to block nicotine's antinociception (in two tests), motor effects, hypothermia, and convulsive effectswith different potencies in the present investigation, suggesting that bupropion possesses some selectivity for neuronal nicotinic receptors underlying these various nicotinic effects. In addition, bupropion blocks nicotine activation of alpha(3)beta(2), alpha(4)beta(2), and alpha(7) neuronal acetylcholine nicotinic receptors (nAChRs) with some degree of selectivity. It was similar to 50 and 12 times more effective in blocking alpha(3)beta(2) and alpha(4)beta(2) than alpha(7). This functional blockade was noncompetitive, because it was insurmountable by increasing concentration of ACh in the nAChRs subtypes tested. Furthermore, bupropion at high concentration failedto displace brain [H-3]nicotine binding sites, a site largely composed of alpha(4)beta(2) subunit combination. Given the observation that bupropion inhibition of alpha(3)beta(2) and alpha(4)beta(2) receptors exhibits voltage-independence properties, bupropion may not be acting as an open channel blocker. These effects may explain in part bupropion's efficacy in nicotine dependence. Our present findings suggest that functional blockade of neuronal nAChRs are useful in nicotine dependence treatment.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 22/09/20 alle ore 15:23:26