(C) 2007 Elsevier Ltd. All fights reserved.”
“The cannabinoid receptor subtype (CB I) antagonist rimonabant (SR141716) has been shown to decrease nicotine self-administration and attenuate nicotine-evoked

dopamine release in the nucleus accumbens; effects that support recent findings on its clinical efficacy as a smoking cessation aid. The present experiments aim to advance our understanding on the role of CB1 receptors in rodent models of nicotine dependence. AM251. a selective antagonist at CB1 receptors dose-dependently (1, 3 and 10 mg/kg IP) suppressed https://www.selleckchem.com/products/lb-100.html intravenous nicotine (0.03 mg/kg per infusion) self-administration in rats during three successive days of pre-treatment. This

reduction was short lasting since behaviour was reinstated by suspending AM251 pre-treatment. This was relatively specific to nicotine LY2874455 mw self-administration since the profile of these reductions produced by AM251 was significantly different from the responses maintained by food pellets. In a model of nicotine-seeking behaviour, rats that had been extinguished by removal of nicotine and associated cues, and presented with a priming dose of nicotine (0.2 mg/kg SC) with the cues, showed robustly reinstated responses to nicotine-seeking behaviour. Acute pre-treatment with AM251 (1-10 mg/kg IP) dose-dependently attenuated the reinstatement effects produced by nicotine and the contingently presented cues. These preclinical findings support the use of rimonabant as a smoking cessation aid and highlight the

CB1 receptor as a viable target to control intake of nicotine and prevent relapse. (C) 2007 Elsevier Ltd. All rights reserved.”
“The nucleus of the solitary tract (NTS) is the principal integrating relay in the processing of visceral sensory and gustatory information. In the present study, patch-clamp electrophysiological experiments were conducted using rat horizontal brainstem sections. Pre-synaptic and somatic/dendritic nicotinic acetylcholine receptors (nAChRs) expressed in neurons of the caudal NTS (cNTS) were Stattic cell line found to be randomly distributed between pre-synaptic and somatic/dendritic sites (chi(2) = 0.72, df = 3, p > 0.87, n = 200). Pre-synaptic nAChRs were detected by their facilitating effects on glutamatergic neurotransmission of a sub-population of cNTS neurons (categorized as “”effect-positive”") upon brief picospritzer applications of 0.1-0.5 mM nicotine. These effects were resistant to inhibition by 20 nM methyllycaconitine (MLA) and 4 mu M dihydro-beta-erythroidine (DH beta E), and were replicated by brief picospritzer applications of 0.2-1 mM cytisine. Picospritzer applications of 0.2 mM RJR-2403, a potent agonist of alpha 4 beta 2 nAChRs, did not facilitate synaptic release of glutamate in effect-positive cNTS neurons.