STRESS-INDUCED DOPAMINE RELEASE IN THE NEOSTRIATUM - EVALUATION OF THE ROLE OF ACTION-POTENTIALS IN NIGROSTRIATAL DOPAMINE NEURONS OR LOCALINITIATION BY ENDOGENOUS EXCITATORY AMINO-ACIDS

It has been hypothesized that excitatory amino acids can initiate dopa mine release in neostriatum. We examined whether the increase in extra cellular dopamine in neostriatum produced by acute stress reflects pre synaptic initiation of dopamine release by endogenous excitatory amino acids. Thirty minutes of intermittent tail-shock stress significantly elevated extracellular concentrations of dopamine, glutamate, asparta te, and gamma-aminobutyric acid in neostriatum of freely moving rats a s measured with in vivo microdialysis. Local infusion of the N-methyl- D-asparatate receptor antagonist 2-amino-5-phosphonovalerate or the no n-N-methyl-D-aspartate receptor antagonist 6-cyano-7-nitroquinoxaline- 2,3-dione via the dialysis probe did not attenuate the stress-induced increase in extracellular dopamine. In fact, the increase was prolonge d in rats treated with specific excitatory amino acid receptor antagon ists. Infusion of tetrodotoxin into medial forebrain bundle increased extracellular glutamate and aspartate in neostriatum yet reduced basal dopamine in extracellular fluid to below the limit of detection of th e assay and eliminated the stress-induced increase in extracellular do pamine. These findings fail to support the hypothesis that the stress- induced increase in extracellular dopamine in neostriatum is initiated locally by excitatory amino acids. Rather, the effects of stress on e xtracellular dopamine seem to be determined by impulse propagation in dopamine neurons.