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Modulation of Dendritic Release of Dopamine by N ‐Methyl‐D‐Aspartate Receptors in Rat Substantia Nigra
Author(s) -
Araneda Ricardo,
Bustos Gonzalo
Publication year - 1989
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.1471-4159.1989.tb02548.x
Subject(s) - kainate receptor , nmda receptor , chemistry , substantia nigra , glutamate receptor , dopamine , strychnine , medicine , tetrodotoxin , receptor , endocrinology , biophysics , ampa receptor , biology , biochemistry , dopaminergic
A superfusion system was used to study the effects of excitatory amino acids (EAA) on release of [ 3 H]dopamine ([ 3 H]DA) previously taken up by rat substantia nigra (SN) slices. The EAA tested (20–250 μM ), with the exception of quisqualate and kainate, markedly evoked [ 3 H]DA release from nigral slices when Mg 2+ ions were omitted from the superfusion medium. The EAA receptor agonists exhibited the following relative potency in stimulating [ 3 H]DA release: l ‐glutamate (L‐Glu) > N ‐methyl‐ d ‐aspartate (NMDA) > NM(D,L)A > d ‐Glu ≫ quisqualate = kainate. d ‐2‐Amino‐5‐phosphonovalerate (100–200 μ.M ), an antagonist for NMDA receptors, substantially reduced [ 3 H]DA release evoked by l ‐Glu or NMDA. In contrast, l ‐Glu diethyl ester (100–200 μM ) produced a lesser blocking effect on [ 3 H]DA release evoked by the EAA. Further experiments showed that the NMDA‐mediated release of [ 3 H]DA was totally suppressed by the omission of Ca 2+ or by the addition of tetrodotoxin (0.1 μM ) to the superfusion medium. In addition, strychnine, an antagonist for glycine (Gly) receptors, significantly decreased NMDA (100 μM )‐evoked as well as glycine (100 μM ‐evoked release of [ 3 H]DA from nigral slices. The results shown support the idea that activation of NMDA subtype receptors in SN may trigger a Ca 2+ ‐dependent release of DA from dendrites of nigro‐striatal DA‐containing neurons. Furthermore, a transsynaptic mechanism that may partially involve Gly‐containing interneurons is proposed to account for some of the events mediating NMDA receptor activation and DA release in SN.