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Nicotinic acetylcholine receptors in the anterior, but not posterior, ventral tegmental area mediate ethanol-induced elevation of accumbal dopamine levels.

Artikel i vetenskaplig tidskrift
Författare Mia Ericson
Elin Löf
Rosita Stomberg
Pei Pei Chau
Bo Söderpalm
Publicerad i The Journal of pharmacology and experimental therapeutics
Volym 326
Nummer/häfte 1
Sidor 76-82
ISSN 1521-0103
Publiceringsår 2008
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi
Sidor 76-82
Språk en
Länkar dx.doi.org/10.1124/jpet.108.137489
Ämnesord Animals, Dopamine, metabolism, Ethanol, administration & dosage, Male, Microdialysis, methods, Nucleus Accumbens, drug effects, metabolism, Rats, Rats, Wistar, Receptors, Nicotinic, metabolism, Ventral Tegmental Area, drug effects, metabolism
Ämneskategorier Farmakologi, Biologisk beroendeforskning, Neurobiologi, Beroendelära

Sammanfattning

Ethanol-induced elevations of accumbal dopamine levels have been linked to the reinforcing properties of the drug. However, it has not yet been demonstrated where the primary point of action of ethanol is in the mesolimbic dopamine system, and there appear to be conflicting findings depending on methodology (electrophysiology, microdialysis, or intracranial self-administration). We have suggested that ethanol acts in the nucleus accumbens (nAc), where it activates a neuronal loop involving ventral tegmental nicotinic acetylcholine receptors (nAChRs) to elevate dopamine levels in the nAc. Application of ethanol in the nAc results in elevated dopamine levels in the same brain region, whereas administration in the anterior ventral tegmental area (VTA) fails to influence dopamine output. In the present study, we were able to repeat these findings. In addition, application of ethanol in the posterior VTA also failed to influence nAc dopamine levels. Perfusion of the nAChR antagonist mecamylamine in the anterior VTA completely blocked the elevation of accumbal dopamine levels observed after ethanol perfusion in nAc, whereas mecamylamine in the posterior VTA had no effect. To detect a possible influence on phasic dopamine release, the dopamine transporter inhibitor nomifensine was included in the accumbal perfusate. In addition, under these conditions, ethanol in the anterior or posterior VTA failed to influence dopamine release in the nAc. These results support previous suggestions of distinct functions of the anterior and posterior VTA and give further evidence for our hypothesis of a nAc-anterior VTA-nAc neuronal circuitry involved in the dopamine-activating effects of ethanol.

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