Abstract:
:A push-pull cannula supplied with artificial CSF was implanted in the striatum of anaesthetized rats, and the basal extracellular DA and DOPAC was assayed in the superfusates using HPLC and electrochemical detection. Simultaneously, a carbon fibre electrode was implanted in close proximity of the cannula and the evoked DA release was detected by differential pulse amperometry during stimulation of the DA axons. Local treatments with cadmium (100 microM) blocked the evoked DA release (-90%), but substantially increased the basal extracellular DA (+125%). The effects of glutamate agonists NMDA (1 mM) and kainate (0.1 mM), known to increase basal extracellular DA were confirmed (+150% and +60% respectively). It was, however, simultaneously observed that the evoked DA release was inhibited (-80% and -50%, respectively). Amphetamine (1 microM) released DA (+150%) and produced also an increase (+100%) of the evoked DA release. These results, apparently conflicting, show that the two mechanisms releasing dopamine (firing-dependent and not) can be directly and simultaneously observed. These two releasing processes appear to be not strictly antagonist. They are also differently and independently modulated by calcium and by local influences such those conveyed by glutamate.
journal_name
Brain Resjournal_title
Brain researchauthors
Olivier V,Guibert B,Leviel Vdoi
10.1016/0006-8993(95)00706-vsubject
Has Abstractpub_date
1995-10-09 00:00:00pages
1-9issue
1eissn
0006-8993issn
1872-6240pii
0006-8993(95)00706-Vjournal_volume
695pub_type
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