The effects of intra-accumbal administration of the nicotinic acetylcholine receptor agonist cytisine on the operant oral self-administration of ethanol were prevented by the GABAB receptor agonist baclofen in rats.

Rationale: Although the mesocorticolimbic dopamine (DA) system is the main neurochemical substrate that regulates the addictive and reinforcing effects of ethanol (EtOH), other neurotransmitter systems, such as the acetylcholine (Ach) system, modulate DAergic function in the nucleus accumbens (nAcc). Previously, we reported that intra-nAcc administration of the nicotinic Ach receptor agonist cytisine increased oral EtOH self-administration. GABAB receptors in the nAcc are expressed in DAergic terminals, inhibit the regulation of DA release into the nAcc, and could modulate the effects of cytisine on oral EtOH self-administration.

Role of drug-associated environmental stimuli in the development of cross-tolerance to the tachycardic effects of nicotine and alcohol in humans.

According to the Pavlovian conditioning model, drug tolerance is modulated by drug-associated environmental cues. This study evaluated the contribution of drug-associated cues in the development of cross-tolerance to the tachycardic effects of nicotine from tobacco and alcohol in human subjects. Forty undergraduate students were recruited for this experiment, and each student was randomly assigned to one of two experimental conditions.

Effect of coadministration of the GABA agonist baclofen and the 5-HT agonist Ro60-0175 on the expression of amphetamine-induced locomotor sensitization.

GABA and 5-HT agonists are effective in attenuating the behavioral effects of psychostimulants. However, they induce adverse side effects when used in high doses. The previous evidence has suggested that the 5HT receptor activation effect could be produced by an increased release of GABA in the ventral tegmental area (VTA) and the consequent activation of GABAergic receptors.