Taurine elevates dopamine levels in the rat nucleus accumbens; antagonism by strychnine

Authors

  • Mia Ericson,

    1. Institute of Neuroscience and Physiology, Section of Psychiatry and Neurochemistry, The Sahlgrenska Academy at Göteborg University, Blå Stråket 15, 413 45, Göteborg, Sweden
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  • Anna Molander,

    1. Institute of Neuroscience and Physiology, Section of Psychiatry and Neurochemistry, The Sahlgrenska Academy at Göteborg University, Blå Stråket 15, 413 45, Göteborg, Sweden
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  • Rosita Stomberg,

    1. Institute of Neuroscience and Physiology, Section of Psychiatry and Neurochemistry, The Sahlgrenska Academy at Göteborg University, Blå Stråket 15, 413 45, Göteborg, Sweden
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  • Bo Söderpalm

    1. Institute of Neuroscience and Physiology, Section of Psychiatry and Neurochemistry, The Sahlgrenska Academy at Göteborg University, Blå Stråket 15, 413 45, Göteborg, Sweden
    2. Beroendekliniken, Sahlgrenska University Hospital, Göteborg, Sweden
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Dr Mia Ericson, Institute of Neuroscience and Physiology, Section of Psychiatry and Neurochemistry, Blå Stråket 15, 413 45 Göteborg, Sweden.
E-mail: mia.ericson@neuro.gu.se

Abstract

The mesolimbic dopamine (DA) system, projecting from the ventral tegmental area (VTA) to the nucleus accumbens (nAcc), is involved in reward-related behaviours and addictive processes, such as alcoholism and drug addiction. It was recently suggested that strychnine-sensitive glycine receptors (GlyR) in the nAcc regulate both basal and ethanol-induced mesolimbic DA activity via a neuronal loop involving endogenous activation of nicotinic acetylcholine receptors (nAChR) in the VTA. However, as the nAcc appears to contain few glycine-immunoreactive cell bodies or fibres, the question as to what may be the endogenous ligand for GlyRs in this brain region remains open. Here we have investigated whether the amino acid taurine could serve this purpose using in vivo microdialysis in awake, freely moving male Wistar rats. Local perfusion of taurine (1, 10 or 100 mm in the perfusate) increased DA levels in the nAcc. The taurine (10 mm)-induced DA increase was, similarly to that previously observed after ethanol, completely blocked by (i) perfusion of the competitive GlyR antagonist strychnine in the nAcc, (ii) perfusion of the nAChR antagonist mecamylamine (100 µm) in the VTA, and (iii) systemic administration of the acetylcholine-depleting drug vesamicol (0.4 mg/kg, i.p). The present results suggest that taurine may be an endogenous ligand for GlyRs in the nAcc and that the taurine-induced elevation of DA levels in this area, similarly to that observed after local ethanol, is mediated via a neuronal loop involving endogenous activation of nAChRs in the VTA.

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