Premium
Glutamate Stimulation of [ 3 H]Dopamine Release from Dissociated Cell Cultures of Rat Ventral Mesencephalon
Author(s) -
Mount H.,
Welner S.,
Quirion R.,
Boksa P.
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.tb01879.x
Subject(s) - dopamine , glutamate receptor , stimulation , veratridine , chemistry , biology , medicine , endocrinology , biochemistry , biophysics , sodium , receptor , sodium channel , organic chemistry
Abstract In dissociated cell cultures of fetal rat ventral mesencephalon preloaded with [ 3 H]dopamine, glutamate (10 ‐5 ‐10 ‐3 M ) stimulated the release of [ 3 H]dopamine. Glutamate stimulation of [ 3 H]dopamine release was Ca 2+ dependent and was blocked by the glutamate antagonist, cis ‐2,3‐piperidine dicarboxylic acid. Glutamate stimulation of [ 3 H]dopamine release was not due to glutamate neurotoxicity because (1) glutamate did not cause release of a cytosolic marker, lactate dehydrogenase, and (2) preincubation of cultures with glutamate did not impair subsequent ability of the cells to take up or release [ 3 H]dopamine. Thus, these dissociated cell cultures appear to provide a good model system to characterize glutamate stimulation of dopamine release. Release of [ 3 H]dopamine from these cultures was stimulated by verat‐ridine, an activator of voltage‐sensitive Na + channels, and this stimulation was blocked by tetrodotoxin. However, glutamate stimulated [ 3 H]dopamine release was not blocked by tetrodotoxin or Zn 2+ . Substitution of NaCl in the extracellular medium by sucrose, LiCl, or Na 2 SO 4 had no effect on glutamate stimulation of [ 3 H]dopamine release; however, release was inhibited when NaCl was replaced by choline chloride or N ‐methyl‐ d ‐glucamine HCl. Glutamate‐stimulated [ 3 H]‐dopamine release was well maintained (60‐82% of control) in the presence of Co 2+ , which blocks Ca 2+ action potentials, and was unaffected by the local anesthetic, lidocaine. These results are discussed in terms of the receptor and ionic mechanisms involved in the stimulation of dopamine release by excitatory amino acids.