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      beta-Alanine elevates dopamine levels in the rat nucleus accumbens: antagonism by strychnine.

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      Animals, Dopamine, metabolism, Dose-Response Relationship, Drug, Extracellular Fluid, Glycine Agents, pharmacology, Ligands, Male, Microdialysis, Neurons, drug effects, secretion, Nucleus Accumbens, Perfusion, Rats, Rats, Wistar, Receptors, Glycine, antagonists & inhibitors, physiology, Strychnine, administration & dosage, Time Factors, beta-Alanine

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          Abstract

          Glycine receptors (GlyRs) in the nucleus accumbens (nAc) have recently been suggested to be involved in the reinforcing and dopamine-elevating properties of ethanol via a neuronal circuitry involving the VTA. Apart from ethanol, both glycine and taurine have the ability to modulate dopamine output via GlyRs in the same brain region. In the present study, we wanted to explore whether yet another endogenous ligand for the GlyR, beta-alanine, had similar effects. To this end, we monitored dopamine in the nAc by means of in vivo microdialysis and found that local perfusion of beta-alanine increased dopamine output. In line with previous observations investigating ethanol, glycine and taurine, the competitive GlyR antagonist strychnine completely blocked the dopamine elevation. The present results suggest that beta-alanine has the ability to modulate dopamine levels in the nAc via strychnine-sensitive GlyRs, and are consistent with previous studies suggesting the importance of this receptor for modulating dopamine output.

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