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Rising taurine and ethanol concentrations in nucleus accumbens interact to produce dopamine release after ethanol administration.

Artikel i vetenskaplig tidskrift
Författare Mia Ericson
Pei Pei Chau
Rhona B. C. Clarke
Louise Adermark
Bo Söderpalm
Publicerad i Addiction biology
Volym 16
Nummer/häfte 3
Sidor 377-385
ISSN 1369-1600
Publiceringsår 2011
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi
Sidor 377-385
Språk en
Länkar dx.doi.org/10.1111/j.1369-1600.2010...
Ämnesord Alcohol; glycine receptor; microdialysis; nucleus accumbens; rat; taurine
Ämneskategorier Farmakologi, Beroendelära

Sammanfattning

We have previously demonstrated that glycine receptors in the nucleus accumbens (nAc) are involved in modulating both basal and ethanol-induced dopamine output in the same brain region. Ethanol is known to induce a release of both taurine and dopamine in the nAc, but the relationship between these two neuromodulators has not been investigated thoroughly. In vivo microdialysis was used to measure the effects of systemic ethanol diluted in isotonic (0.9% NaCl) or hypertonic (3.6% NaCl) saline on accumbal taurine and dopamine levels. We found that ethanol given in a hypertonic solution, contrary to an isotonic solution, failed to increase concentrations both of taurine and dopamine in the nAc. However, a modest, non-dopamine elevating concentration of taurine in the nAc disclosed a dopamine-elevating effect of systemic ethanol also when given in a hypertonic solution. In a second experiment, we investigated the effects of ethanol on taurine and dopamine in normal rats and rats with decreased levels of endogenous taurine. Lowering the level of taurine, approximately 40% by adding 5% β-alanine in the drinking water, did not influence taurine or dopamine output over time. We conclude that the elevations of taurine and dopamine in the nAc are closely related, and that in order for ethanol to induce dopamine release, a simultaneous increase of extracellular taurine levels in the nAc is required. These data also provide support for the notion that the nAc is the primary target for ethanol in its dopamine-activating effect after systemic administration.

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