Abstract
The goal of this review is to describe what the voltammetry technique tells us about cocaine–dopamine transporter (DAT) interactions and the subsequent changes in extracellular dopamine levels in the brain. The primary advantage of voltammetry, in this regard, is the capability for kinetic analysis in situ. Analysis of electrically evoked dynamics suggests that cocaine competitively inhibits dopamine uptake in the caudate-putamen and nucleus accumbens with a similar efficacy. The preferential increase in accumbal dopamine following systemic cocaine administration was found to be related not to a unique cocaine–DAT interaction, but rather to a unique combination of dopamine release and uptake rates. Similar enhancement occurs in sub-regions of the caudate-putamen exhibiting this release and uptake combination. Other factors such as diffusion and whether dopaminergic signaling is tonic or phasic also determine the effects of cocaine on striatal dopamine levels.
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