RECIPROCAL INTERACTION BETWEEN GLUTAMATE AND DOPAMINE IN THE PARS RETICULATA OF THE RAT SUBSTANTIA-NIGRA - A MICRODIALYSIS STUDY

Citation
Mg. Rosales et al., RECIPROCAL INTERACTION BETWEEN GLUTAMATE AND DOPAMINE IN THE PARS RETICULATA OF THE RAT SUBSTANTIA-NIGRA - A MICRODIALYSIS STUDY, Neuroscience, 80(3), 1997, pp. 803-810
Citations number
45
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
03064522
Volume
80
Issue
3
Year of publication
1997
Pages
803 - 810
Database
ISI
SICI code
0306-4522(1997)80:3<803:RIBGAD>2.0.ZU;2-O
Abstract
We studied the interactions between glutamate and dopamine in the pars reticulata of the substantia nigra by using microdialysis in unanaest hetized rats. Increased extracellular levels of glutamate in the pars reticulata were obtained by microinjecting the muscarinic agonist carb achol into the ipsilateral subthalamic nucleus. The increase of glutam ate levels was followed by increments in extracellular levels of dopam ine and GABA. Increased levels of the three neurotransmitters were als o observed during the administration of N-methyl-D-aspartate through t he microdialysis probe. The increase in glutamate and GABA caused by N -methyl-D-aspartate was blocked by SCH 23390, a selective D-1 antagoni st. However, the D-1 antagonist did not prevent the increase in dopami ne levels. The selective D-1 agonist SKF 38393, added to the microdial ysis probe, increased the levels of the three neurotransmitters. Howev er, after the lesion of the subthalamic nucleus with kainic acid, SKF 38393 increased only the level of GABA but not those of glutamate and dopamine. In addition, the lesion of the subthalamic nucleus produced a drastic (80%) fall in the extracellular levels of glutamate. These d ata suggest that glutamate, through N-methyl-d-aspartate receptors, st imulates the release of dopamine from dopaminergic dendrites present i n the substantia nigra pars reticulata, and that dopamine in turn stim ulates the release of glutamate and GABA. Both effects are mediated by D-1 dopamine receptors present on subthalamonigral and striatonigral axon terminals, respectively. (C) 1997 IBRO. Published by Elsevier Sci ence Ltd.