title: Striatal interaction among dopamine, glutamate and ascorbate.
abstract: Despite evidence suggesting the interaction among glutamate (GLU), dopamine (DA) and ascorbic acid (AA) in the striatum, their actions are often studied separately. Microdialysis was used here to quantify the extracellular interaction among GLU-DA-AA in the striatum of rats, an interaction which was compared with those studied in the substantia nigra (SN). Perfusion of GLU by reverse microdialysis increased DA and decreased 3,4-dihydroxyphenylacetic acid (DOPAC) in the extracellular medium of the striatum, but increased both DA and DOPAC in the SN. The increase of extracellular DA-concentration induced by the local DA-perfusion decreased the extracellular level of GLU and glutamine, an effect that, as suggested by the GLU and glutamine increase observed after the haloperidol administration, probably involves the D2 dopamine receptor. Local administration of AA increased the extracellular DA, decreased DOPAC and had no effect on GLU and glutamine. Present data suggest that, in the striatum, GLU-release inhibits DA-uptake, DA-release inhibits GLU-release, and AA-release prevents DA-oxidation increasing its extracellular diffusion. These effects were different in the SN where GLU probably promoted the DA-release instead of inhibiting the DA-uptake as presumably occurred in the striatum. Present data denote a marked GLU-DA-AA interaction in the striatum, which might be relevant for the pharmacological control of basal ganglia disorders.
authors.affiliation: Laboratory of Neurobiology and Experimental Neurology, Department of Physiology, Faculty of Medicine, University of La Laguna, La Laguna, Tenerife, Canary Islands, Spain.
authors.forename: Ingrid
authors.initials: I
authors.lastname: Morales
authors.forename: Angel
authors.initials: A
authors.lastname: Fuentes
authors.forename: Santiago
authors.initials: S
authors.lastname: Ballaz
authors.forename: Jose A
authors.initials: JA
authors.lastname: Obeso
authors.forename: Manuel
authors.initials: M
authors.lastname: Rodriguez
mesh_terms: D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000378:metabolism* / Q000494:pharmacology; D001205:Ascorbic Acid / Q000008:administration & dosage / Q000378:metabolism* / Q000494:pharmacology; D001480:Basal Ganglia Diseases / Q000503:physiopathology; D002851:Chromatography, High Pressure Liquid; D004298:Dopamine / Q000008:administration & dosage / Q000378:metabolism* / Q000494:pharmacology; D015259:Dopamine Agents / Q000494:pharmacology; D018492:Dopamine Antagonists / Q000494:pharmacology; D004563:Electrochemistry; D005470:Fluorometry; D018698:Glutamic Acid / Q000008:administration & dosage / Q000378:metabolism* / Q000494:pharmacology; D006220:Haloperidol / Q000494:pharmacology; D007980:Levodopa / Q000494:pharmacology; D008297:Male; D017551:Microdialysis; D017072:Neostriatum / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000975:Antioxidants; D015259:Dopamine Agents; D018492:Dopamine Antagonists; D015102:3,4-Dihydroxyphenylacetic Acid; D018698:Glutamic Acid; D007980:Levodopa; D006220:Haloperidol; D001205:Ascorbic Acid; D004298:Dopamine