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Characterization of ethanol-induced dopamine elevation in the rat nucleus accumbens.

Artikel i vetenskaplig tidskrift
Författare Elin Löf
Mia Ericson
Rosita Stomberg
Bo Söderpalm
Publicerad i European journal of pharmacology
Volym 555
Nummer/häfte 2-3
Sidor 148-55
ISSN 0014-2999
Publiceringsår 2007
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi
Institutionen för neurovetenskap och fysiologi, sektionen för farmakologi
Sidor 148-55
Språk en
Länkar dx.doi.org/10.1016/j.ejphar.2006.10...
Ämnesord Animals, Central Nervous System Depressants, administration & dosage, Dopamine, biosynthesis, Ethanol, administration & dosage, GABA Antagonists, pharmacology, Male, Microdialysis, Nucleus Accumbens, drug effects, metabolism, Picrotoxin, pharmacology, Rats, Rats, Wistar, Receptors, GABA-A, antagonists & inhibitors, metabolism, Ventral Tegmental Area, drug effects, metabolism
Ämneskategorier Farmakologi, Biologisk beroendeforskning, Neurobiologi, Beroendelära

Sammanfattning

Ethanol-induced accumbal dopamine elevations have been linked to ethanol consumption. It is unclear, however, where along the mesolimbic dopamine system this effect is initiated and why the ethanol-induced dopamine elevations are transient, returning to pre-drug baseline before brain and blood ethanol levels decline. Using in vivo microdialysis, Experiment 1 investigated the effect of local ethanol application in the nucleus accumbens, the ventral tegmental area and the nucleus accumbens+the ventral tegmental area, on accumbal dopamine. Experiment 2 examined whether the rapid withdrawal of dopamine response to ethanol involves activation of GABA(A)-receptors, by analyzing the effect of accumbal co-perfusion of picrotoxin and ethanol. In Experiment 1, ethanol perfusion into the ventral tegmental area alone did not affect accumbal dopamine. Ethanol co-perfusion of one of the tested doses into the ventral tegmental+the nucleus accumbens produced higher dopamine levels than ethanol perfusion into the nucleus accumbens alone during 120-160 min following perfusion onset. In Experiment 2, accumbal ethanol perfusion caused a transient increase in nucleus accumbens dopamine. Co-perfusion of ethanol and picrotoxin produced a sustained dopamine elevation. These data support the hypothesis that the primary effect of ethanol on accumbal dopamine is in the nucleus accumbens, but that a secondary effect of nucleus accumbens ethanol perfusion, such as release of acetylcholine in the ventral tegmental area, enables ethanol to act as a nicotinic acetylcholine receptor co-agonist in this area. Moreover, recruitment of GABA(A)-receptor activity appears responsible for the second, declining phase with respect to dopamine levels following ethanol administration.

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