Changed accumbal responsiveness to alcohol in rats pre-treated with nicotine or the cannabinoid receptor agonist WIN 55,212-2
Section snippets
Acknowledgements
This work was supported by The European Fith Framework Programme QLRT-2000-01691, Ministerio de Ciencia y Tecnología Grant BFI-2001-C02-01, Fondo de Investigación Sanitaria (Red Trastornos Adictivos), M.S.C (Plan Nacional Sobre Drogas), M.E.C.
References (41)
- et al.
Neuromodulatory role of the endocannabinoid signaling system in alcoholism: an overview
Prostaglandins Leukot. Essent. Fatty Acids
(2002) - et al.
Accumbal dopamine overflow after ethanol: localization of the antagonizing effect of mecamylamine
Eur. J. Pharmacol.
(1997) - et al.
The dopamine-containing neuron: maestro or simple musician in the orchestra of addiction?
Trends Pharmacol. Sci.
(2003) - et al.
Ethanol modulates nicotine-induced upregulation of nAChRs
Brain Res.
(2003) - et al.
Ethanol elevates accumbal dopamine levels via indirect activation of ventral tegmental nicotinic acetylcholine receptors
Eur. J. Pharmacol.
(2003) - et al.
The role of mesolimbic dopamine in the development and maintenance of ethanol reinforcement
Pharmacol. Ther.
(2004) Memory and addiction: shared neural circuitry and molecular mechanisms
Neuron
(2004)- et al.
Nicotine-induced changes of glutamate and arginine in naive and chronically alcoholized rats: an in vivo microdialysis study
Brain Res.
(2006) - et al.
Nicotine in alcohol deprivation increases alcohol operant self-administration during reinstatement
Neuropharmacology
(2004) - et al.
Alcohol dependence is associated with blunted dopamine transmission in the ventral striatum
Biol. Psychiatry
(2005 Nov 15)
Long-term reduction in ventral tegmental area dopamine neuron population activity following repeated stimulant or ethanol treatment
Biol. Psychiatry
Nicotinic mechanisms involved in the dopamine activating and reinforcing properties of ethanol
Behav. Brain Res.
Measurement of the striatal dopamine transporter density and heterogeneity intype 1 alcoholics using human whole hemisphere autoradiography
Neuroimage
Dopamine: the salient issue
Trends Neurosci.
The endocannabinoid system in the basal ganglia and in the mesolimbic reward system: implications for neurological and psychiatric disorders
Eur. J. Pharmacol.
WIN 55,212-2 decreases the reinforcing actions of cocaine through CB1 cannabinoid receptor stimulation
Behav. Brain Res.
Cannabis induced dopamine release: an in vivo SPECT study
Psychiatry Res.
Changes in cigarette smoking and coffee drinking after alcohol detoxification in alcoholics
Addiction
Alcohol promotes dopamine release in the human nucleus accumbens
Synapse
Cannabinoids enhance subsecond dopamine release in the nucleus accumbens of awake rats
J. Neurosci.
Cited by (19)
The incentive amplifying effects of nicotine: Roles in alcohol seeking and consumption
2022, Advances in PharmacologyCitation Excerpt :As discussed previously, nicotine appears to better enhance voluntary alcohol intake when it is given in exposure windows either developmentally or temporally dissociated from the period of alcohol consumption. In contrast to the previously described studies, subchronic nicotine can actually blunt alcohol-induced DA release in the NAccSh (Lopez-Moreno et al., 2008). The effect of nicotine pre-exposure can persist long after it is metabolized, attenuating the alcohol-induced release of NAcc DA and VTA firing, while producing concurrent increases in alcohol consumption (Doyon, Dong, et al., 2013).
Critical needs in drug discovery for cessation of alcohol and nicotine polysubstance abuse
2016, Progress in Neuro-Psychopharmacology and Biological PsychiatryCitation Excerpt :That is, simultaneous co-administration of nicotine and alcohol produces an additive increase in NAc dopamine release relative to the response of each drug (Tizabi et al., 2002; Doyon et al., 2013a, 2013b). Perhaps surprisingly, pretreatment with nicotine diminishes the sensitivity of the mesolimbic dopamine system to alcohol (Lopez-Moreno et al., 2008; Doyon et al., 2013a, 2013b; Ostroumov et al., 2015). An acute 3, 15 or 40 h pretreatment with nicotine (0.4 mg/kg, ip) significantly blunted the alcohol (1.5 g/kg, iv)-induced increase in dopamine release in rat NAc (Doyon et al., 2013a, 2013b).
Cigarettes and alcohol: The influence of nicotine on operant alcohol self-administration and the mesolimbic dopamine system
2015, Biochemical PharmacologyCitation Excerpt :The nicotine and ethanol interaction has been shown to activate a set of interconnected brain structures involved in stress and reward processing, including the ventral tegmental area (VTA), nucleus accumbens, dorsomedial prefrontal cortex, and extended amygdala [63]. Pretreatment with nicotine has been shown to decrease the responsiveness of the DA system to ethanol [22,79]. We have shown that pretreatment with nicotine (3–40 h prior to testing) decreases the amplitude and the time course of ethanol-induced DA signals in the VTA and the nucleus accumbens when compared to control animals pretreated with saline [22].
Potential substrates for nicotine and alcohol interactions: A focus on the mesocorticolimbic dopamine system
2013, Biochemical PharmacologyCitation Excerpt :Local blockade of CB1 receptors in the VTA and the NAc reduces alcohol consumption, suggesting a critical role of eCB signaling in the mesoaccumbens pathway [233]. Pretreatment with a CB1 receptor agonist or with nicotine blocked alcohol-induced DA release, suggesting that these agents may interact with alcohol through a common mechanism [105]. In addition, alcohol increases conditioned place preference induced by nicotine, and this effect is prevented by blocking eCB receptors [234].
- 1
Both authors have participated equally to this work.