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Pre‐synaptic glutamate‐induced activation of DA release in the striatum after partial nigral lesion
Author(s) -
Dzahini Kwamivi,
Dentresangle Christine,
Le Cavorsin Marion,
Bertrand Anne,
Detraz Isabelle,
Savasta Marc,
Leviel Vincent
Publication year - 2010
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2010.06682.x
Subject(s) - glutamate receptor , striatum , neuroscience , lesion , chemistry , biology , dopamine , medicine , biochemistry , pathology , receptor
J. Neurochem. (2010) 113 , 1459–1470. Abstract The present experiments aimed at understanding the functional link between dopamine (DA) and glutamate (GLU) during the compensatory processes taking place after partial DA denervation. Lesion of the lateral part of substantia nigra in rats using 6‐hydroxydopamine resulted in DA denervation of the lateral region of the ipsilateral caudate/putamen complex (CPc) whereas the medial CPc was spared. In vivo voltammetry revealed a large increase of extracellular dopamine (DA ext ) in the medial CPc both ipsilateral and contralateral to the lesion. In addition, in vivo microdialysis and HPLC‐ED revealed a concomitant increase of extracellular glutamate (GLU ext ) in the ipsilateral medial CPc. Post‐lesion chronic treatment with the putative neuroprotectors amantadine, memantine, and riluzole counteracted the tonic increases of DA ext and GLU ext , revealing a possible role of GLU neurotransmission in the DA over‐expression. Finally, acute low doses of GBR12909 had no effect on the DA ext in sham‐ operated animals, but dramatically increased DA ext in lesioned animals. The data suggest that a partial unilateral nigral lesion induces a bilateral increase of DA turn‐over in the non‐denervated striata through GLU afferences to the DA terminals.