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

Artikel i vetenskaplig tidskrift
Författare Mia Ericson
Anna C Molander
Rosita Stomberg
Bo Söderpalm
Publicerad i The European journal of neuroscience
Volym 23
Nummer/häfte 12
Sidor 3225-9
ISSN 0953-816X
Publiceringsår 2006
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi
Sidor 3225-9
Språk en
Länkar dx.doi.org/10.1111/j.1460-9568.2006...
Ämnesord Animals, Dopamine, metabolism, Ganglionic Blockers, metabolism, Glycine Agents, metabolism, Male, Mecamylamine, Microdialysis, Neuromuscular Depolarizing Agents, metabolism, Nucleus Accumbens, anatomy & histology, metabolism, Piperidines, metabolism, Rats, Rats, Wistar, Receptors, Glycine, antagonists & inhibitors, metabolism, Strychnine, metabolism, Taurine, metabolism
Ämneskategorier Farmakologi, Beroendelära

Sammanfattning

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 microm) 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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