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Midbrain dopamine neurons signal rapid information about rewards and reward-related events. It has been suggested that this fast signal may, in fact, be conveyed by co-released glutamate. Evidence that dopamine neurons co-release glutamate comes largely from studies involving cultured neurons or tissue from young animals. Recently, however, it has been shown that this dual glutamatergic/dopaminergic phenotype declines with age, and can be induced by injury, suggesting that it is not a key feature of adult dopamine neurons. Here, we provide further support for this view by showing that dopaminergic axons and terminals in subregions of the adult striatum do not express vesicular glutamate transporters (VGluT1, VGluT2 or VGluT3). Striatal tissue from the adult rat was immunolabelled to reveal tyrosine hydroxylase (TH; biosynthetic enzyme of dopamine) and one of the three known VGluTs. Importantly, we compared the immunogold labelling for each of the VGluTs associated with TH-positive structures with background labelling at the electron microscopic level. In addition, we carried out a subregional analysis of the core and shell of the nucleus accumbens. We found that dopaminergic axons and terminals in the dorsolateral striatum and ventral striatum (nucleus accumbens core and shell) do not express VGluT1, VGluT2 or VGluT3. We conclude, therefore, that in the normal, adult rat striatum, dopaminergic axons do not co-release glutamate.

Original publication




Journal article


Eur J Neurosci

Publication Date





1205 - 1211


Animals, Axons, Corpus Striatum, Dendrites, Dopamine, Glutamic Acid, Immunohistochemistry, Male, Nucleus Accumbens, Rats, Rats, Sprague-Dawley, Tyrosine 3-Monooxygenase, Vesicular Glutamate Transport Protein 1, Vesicular Glutamate Transport Protein 2, Vesicular Glutamate Transport Proteins