Demon Voltammetry and Analysis software: Analysis of cocaine-induced alterations in dopamine signaling using multiple kinetic measures

Abstract

The fast sampling rates of fast scan cyclic voltammetry make it a favorable method for measuring changes in brain monoamine release and uptake kinetics in slice, anesthetized, and freely moving preparations. The most common analysis technique for evaluating changes in dopamine signaling uses well-established Michaelis-Menten kinetic methods that can accurately model dopamine release and uptake parameters across multiple experimental conditions. Nevertheless, over the years, many researchers have turned to other measures to estimate changes in dopamine release and uptake, yet to our knowledge no systematic comparison amongst these measures has been conducted. To address this lack of uniformity in kinetic analyses, we have created the Demon Voltammetry and Analysis software suite, which is freely available to academic and non-profit institutions. Here we present an explanation of the Demon Acquisition and Analysis features, and demonstrate its utility for acquiring voltammetric data under in vitro, in vivo anesthetized, and freely moving conditions. Additionally, the software was used to compare the sensitivity of multiple kinetic measures of release and uptake to cocaine-induced changes in electrically evoked dopamine efflux in nucleus accumbens core slices. Specifically, we examined and compared tau, full width at half height, half-life, T20, T80, slope, peak height, calibrated peak dopamine concentration, and area under the curve to the well-characterized Michaelis-Menten parameters, dopamine per pulse, maximal uptake rate, and apparent affinity. Based on observed results we recommend tau for measuring dopamine uptake and calibrated peak dopamine concentration for measuring dopamine release.

Paradoxical Abatement of Striatal Dopaminergic Transmission by Cocaine and Methylphenidate

“…Few voltammetric studies have already reported similar changes in DA overflow across psychostimulant concentrations, being the inhibitory effect on DA overflow interpreted as secondary to presynaptic D2 autoreceptor activation (21)(22). However, this is not possible because the depression of DA overflow occurs in the presence of the D2 antagonist sulpiride and also in the DAT-CI striatal slices (where an activation of D2 autoreceptors by an enhanced extracellular DA level does not occur).…”

Early-Life Social Isolation Stress Increases Kappa Opioid Receptor Responsiveness and Downregulates the Dopamine System

“…Once the extracellular DA response was stable for three consecutive stimulations, a cumulative concentration response curve of the KOR agonist, U50,488 (10, 30, 100, 300, 1000 nM), was run by bath applying the drug to NAc slices. All FSCV data were analyzed using the Demon Voltammetry and Analysis software (Yorgason et al, 2011). DA-stimulated release parameters were determined from stabilized signals using a Michaelis-Menten kinetics-based algorithm (Ferris et al, 2013).…”

Amphetamine Self-Administration Attenuates Dopamine D2 Autoreceptor Function

“…This was used to convert an electrical current to a DA concentration. Demon Voltammetry and Analysis software (Yorgason et al, 2011) was used to analyze FSCV data. Eighteen hours after the last session of AMPH selfadministration, tissues from the midbrain (including VTA and SN) or the whole striatum (ventral and dorsal striatum) of AMPH self-administering rats and controls were dissected using a rat brain matrix.…”