IN VIVO VOLTAMMETRY AT MODIFIED MICROELECTRODES (ASCORBIC ACID, NAFION

The goals of this research have been the development and application of modified electrodes to monitor chemical events in the brain. The particular target molecules were ascorbic acid, dopamine, and dihydroxyphenylacetic acid (DOPAC). Modified electrodes improve the selectivity of in vivo techniques which provides more certainty in qualitative identification. Improved selectivity has aided the investigation of the dynamics of dopamine release and physiological role of ascorbate in the mammalian brain.;Microdisk and electrochemically modified carbon fiber electrodes have been used to confirm that the concentration of ascorbate increases with systemic administration of amphetamine. A more recent advance in in vivo voltammetric electrode technology, surface modification with a cation-exchange membrane film (Nafion), provides improved selectivity for cations, such as dopamine, relative to ascorbate, DOPAC and other electroactive anions. The voltammetric and temporal responses of the microdisk electrode coated with very thin films of Nafion have shown it to be an excellent probe for in vivo analysis.;In vivo voltammetry in adrenalectomized animals or with infusions of p-hydroxyamphetamine shows that the central nervous system effects of amphetamine are necessary for the release of ascorbate in the neostriatum. Furthermore, enhanced release of ascorbate observed in the neostriatum is not due to actions of amphetamine in the neostriatum but is mediated in the substantia nigra. Characterization of the amphetamine-induced release of ascorbate was also investigated with the combination of in vivo electrochemistry and electrophysiological single-unit recording. The combined techniques suggest that the activity of the neurons in the neostriatum is controlled by the inhibitory influences of dopamine. A definitive investigation into the dynamics of ascorbate in the neostriatum revealed a system that directly controls the amphetamine-induced release. Destruction of the crus cerebri, a neuronal feedback pathway from the neostriatum to the substantia nigra, by electrolytic lesion results in a complete inhibition of the amphetamine-induced release of ascorbate.