Brain Reward Mechanisms Research Articles

Brain reward mechanisms and the neurobiology of craving

Brain reward mechanisms and the neurobiology of craving

Attenuation of drinking sweetened water following calcium channel blockade

Recent reports cite results that both cocaine-induced conditioned place preference and activity stimulation are attenuated by pretreatment with the calcium channel blocker isradipine (ISR) in rats. By blocking voltage-dependent L-type calcium channels, ISR may regulate neural dopamine release that, in turn, decreases the putative rewarding effects mediated by dopaminergic mechanisms. It is known that nonfluid deprived rats avidly consume sweetened fluids; this suggests that the sweet taste is rewarding. Three experiments were conducted to determine the effects of ISR on drinking sweetened and nonflavored water. Experiment 1 was designed to test whether ISR would attenuate the intake of a palatable solution in a dose-dependent manner. To this end, ISR was administered both peripherally (3.0–30 mg/kg) and centrally (0.3–30 μg/rat) prior to a solution of saccharin and d-glucose (S + G) being made available to rats (15 min/day) and intake was recorded. ISR produced dose-dependent decreases (38%–81%) in S + G intake dependent on the route of administration. In Experiment 2, water intake was measured in 18 h water-deprived rats following ISR (10 mg/kg) administration as well as comparing S + G drinking. The effect of two ISR vehicles, dimethyl sulfoxide and Tween 80, upon fluid intake was also determined. ISR injection did not attenuate water intake in 18 h water-deprived rats and the choice of vehicle did not affect the ISR-induced attenuation of S + G drinking. In Experiment 3, a single dose (30 μg) of ICV administered ISR, that attenuated S + G intake by approximately 44%, did not attenuate water intake in 18 h water-deprived rats. Collectively, these findings demonstrate that ISR attenuates palatability-induced drinking that is believed to be regulated by neural dopaminergic systems. These findings suggest that calcium channel blockers may modulate brain reward mechanisms.

Differential effects of short- and long-term antidepressant treatments on the food-induced place preference conditioning in rats

The effect of antidepressant drugs (ADs) on the rewarding properties of food, given to food-deprived rats, was studied with a conditioned place preference paradigm. Repeated (once a day for 4 days) association of an initially non-preferred environment with the presentation of food resulted in development of an increased preferences for that environment. That effect was diminished when each conditioning session was preceded by administration of single doses of imipramine, desipramine, amitriptyline, mianserin and citalopram (short-term treatment). In contrast, long-term treatment (16 days) with the above ADs, as well as repeated (9) applications of electroconvulsive shock significantly enhanced the food-induced place preference conditioning. In a separate experiment it was also found that ADs, used as unconditioned stimuli, produced a conditioned aversion to the environment previously paired with administration of single doses of the drugs. The above findings are discussed in terms of the enhancement by prolonged antidepressant treatments of the brain reward mechanisms.

Actions of drugs of abuse on brain reward systems: A reconsideration with specific attention to alcohol

Research in the areas of intracranial self-stimulation and drug self-administration has provided a substantial data base that has contributed to our understanding of brain reward mechanisms. In a recent article, Wise [83] argued that dopamine is the catecholamine critically involved in the central mediation of reward. The present paper attempts to examine the available data with particular reference to alcohol, but also with reference to opiates, and argues that the reinforcing effects of at least these drugs are primarily and directly mediated by noradrenergic rather than dopaminergic systems in the brain. It also argues, in direct contrast to Wise, that in the context of these drugs, dopamine seems to play a minor if not negligible role.

Potentiation of brain reward mechanisms by psychomotor stimulant drugs

Potentiation of brain reward mechanisms by psychomotor stimulant drugs