![fluorescent control transfectant (A), a nonfluorescent untransfected cell from the toxin transfection dish (B), and a fluorescent toxin-transfected cell (C) were identified. Cells were loaded with dopamine and stimulated with a3s pulse of 100 µM ATP at 100 s following the start of the amperometric recording. All amperometric data were obtained using a 5 µm carbon fiber electrode held at 0.70 V vs. Ag/AgCl (Reproduced from Pflugers Arch. with permission [5].)](https://images.tandf.co.uk/common/jackets/crclarge/978082470/9780824707316.jpg "fluorescent control transfectant (A), a nonfluorescent untransfected cell from the toxin transfection dish (B), and a fluorescent toxin-transfected cell (C) were identified. Cells were loaded with dopamine and stimulated with a3s pulse of 100 µM ATP at 100 s following the start of the amperometric recording. All amperometric data were obtained using a 5 µm carbon fiber electrode held at 0.70 V vs. Ag/AgCl (Reproduced from Pflugers Arch. with permission [5].)")
ABSTRACT
The PC12 cell line has also been used to probe the mechanisms of action of various neurologically active drugs. For instance, Sulzer et al. have investigated the effects of amphetamine on exocytosis from PC12 cells [52]. Two distinct mechanisms of action have been proposed: (1) exchange diffusion [53] and (2) vesicle depletion [54, 55]. The exchange-diffusion model involves the attachment of extracellular amphetamine to the dopamine transporter, and the subsequent transport of amphetamine into the cell while dopamine is simultaneously transported out of the cell. This model appears to predominate at low concentrations of applied amphetamine [52]. The second mechanism of action, apparently operational at high doses, involves the depletion of catecholamine from intracellular storage vesicles followed by reverse transport out of the cell [52]. The amperometric detection of individual exocytosis events at PC12 cells provides a unique method to probe this second mechanism.
