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Mechanistic studies of ethanol's interaction with the mesolimbic dopamine reward system.

Forskningsöversiktsartikel
Författare Bo Söderpalm
Elin Löf
Mia Ericson
Publicerad i Pharmacopsychiatry
Volym 42 Suppl 1
Sidor S87-94
ISSN 1439-0795
Publiceringsår 2009
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi
Sidor S87-94
Språk en
Länkar dx.doi.org/10.1055/s-0029-1220690
Ämnesord Alcohol Drinking, drug therapy, Animals, Dopamine, metabolism, physiology, Ethanol, pharmacology, Humans, Ion Channel Gating, drug effects, Limbic System, drug effects, metabolism, Models, Neurological, Receptors, Glycine, agonists, Receptors, Nicotinic, drug effects, Reward
Ämneskategorier Farmakologi, Beroendelära

Sammanfattning

Alcoholism is a chronic recurring brain disorder causing the afflicted a multitude of social and health problems and enormous costs to society. The psychosocial and pharmacological treatment options available have but small to moderate effect sizes, underlining the great need for new effective remedies. Alcohol like all other drugs of abuse acutely activates the mesolimbic dopamine system and, upon chronic administration, produces functional alterations of this important part of the brain reward system. Available data suggests that the mesolimbic dopamine system is involved both in the positive and negative reinforcing effects of ethanol. It hence becomes imperative to understand how ethanol interferes with this system. Increased knowledge about these mechanisms may open up for new targets for pharmacotherapies. We have investigated the tentative involvement of cys-loop ligand-gated ion-channels, which ethanol is known to interact with in relevant concentrations. Our data indicate that a neuronal circuitry involving glycine receptors in the nucleus accumbens, and, secondarily, nicotinic acetylcholine receptors in the ventral tegmental area is involved in the mesolimbic dopamine activating and reinforcing effects of ethanol. Manipulations of both these receptor populations have the potential to modulate ethanol consumption. The proposed neurocircuitry, has implications for understanding ethanol conditioned dopamine activation, chronic effects of ethanol on the mesolimbic dopamine system and the overall role/importance of dopamine and the nucleus accumbens for the reinforcing effects of ethanol. Computational neuroscience in conjunction with further emperical observations is likely to facilitate this process.

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