Brain Dopamine and Reward

Abstract

While the evidence is strong that dopamine plays some fundamental and special role in the rewarding effects of brain stimulation, psychomotor stimulants, opiates, and food, the exact nature of that role is not clear. One thing is clear: Dopamine is not the only reward transmitter, and dopaminergic neurons are not the final common path for all rewards. Dopamine antagonists and lesions of the dopamine systems appear to spare the rewarding effects of nucleus accumbens and frontal cortex brain stimulation (Simon et al 1979) and certainly spare the rewarding effects of apomorphine (Roberts & Vickers 1988). It is clear that reward circuitry is multisynaptic, and since dopamine cells do not send axons to each other or receive axons from each other, dopamine can at best serve as but a single link in this circuitry. If dopamine is not a final common path for all rewards, could it be an intermediate common path for most rewards? Some workers have argued against such a view, but at present they must do so on incomplete evidence. For example, Phillips (1984) has argued that there must be multiple reward systems, functionally independent and organized in parallel with one another. His primary evidence, however, is the fact that brain stimulation is rewarding at different levels of the nervous system. As we have seen in the case of midline mesencephalic stimulation, the location of the electrode tip in relation to the dopamine cells and fibers tells us little about the role of dopamine in brain stimulation reward. It seems clear that the ventral tegmental dopamine system plays a critical role in midline mesencephalic reward, despite the distance from the electrode tip to the dopamine cells where morphine causes its dopamine-dependent facilitory effects or to the dopamine terminals where low-dose neuroleptics presumably cause theirs. Until pharmacological challenge has been extended to the cases discussed by Phillips, we can only speculate as to the role of dopamine in each of those cases. In the cases where pharmacological challenge has been examined, only nucleus accumbens and frontal cortex have been found to have dopamine-independent reward sites. It is not consistent with the dopamine hypothesis that dopamine-independent reward sites should exist in these areas, since any reward signals carried to nucleus accumbens or frontal cortex by dopamine fibers would-unless we are to believe that reward "happens" at these sites-have to be carried to the next stage of the circuit by nondopaminergic fibers (there are no dopaminergic cell bodies in any of the dopamine terminal areas).(ABSTRACT TRUNCATED AT 400 WORDS)

The DRD2 TaqI-B polymorphism and its relationship to smoking abstinence and withdrawal symptoms

“…The DRD2 TaqI-B genotype and its interactions with treatment, daily abstinence and time were examined, whereas covarying the corresponding mean baseline (À14 to À1 days pre-quit) WSWS or MWSC score, baseline smoking rate (cigarettes/day), daily abstinence, depression history (positive vs negative), sex and race. Significant DRD2 TaqI-B Â time interactions were found for several WSWS scales, including anger, F (1,3854 Figure 2 indicate that those smokers with the B2/ B2 genotype tended to report fewer symptoms as a function of time. No interactions between TaqI-B genotype and either treatment or daily abstinence were found.…”

“…1 The role of genetic factors in these dopaminergic pathways are of interest in identifying risk factors for addiction (e.g., [2][3][4] ). Many genes are involved in the regulation of the dopamine system, and the DRD2 gene is one of the most frequently studied in addictive disorders.…”

The neurobiology of social attachment: A comparative approach to behavioral, neuroanatomical, and neurochemical studies

“…DA, particularly in mesolimbic brain regions, has also been implicated in the mediation of a variety of natural rewards (Wise et al, 1989;Bozarth, 1991) including mating (Everitt, 1990) which facilitates pair bonding (Carter et al, 1990;Williams et al, 1992b;Insel et al, 1995b;Curtis et al, 2003a;Wang et al, 2004). For these reasons, DA was hypothesized to play a role in pair bonding and the DAergic regulation of social attachment has since become an important focus of the field.…”

The Role of Acetylcholine in Cocaine Addiction

“…The rewarding effects of natural reinforcers and addictive drugs, including cocaine, are related to their ability to activate the mesolimbic circuit in the midbrain VTA and stimulate the release of DA within the shell compartment of the NAc (Caine et al, 1997;Wise and Rompre, 1989). Drugs that facilitate DA transmission within the mesolimbic pathway enhance the processes by which otherwise neutral stimuli acquire incentive salience and motivate further drug-seeking behavior (Berridge and Robinson, 1998;Wyvell and Berridge, 2000).…”