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The Journal of Neuroscience, August 15, 2001, 21(16):5916-5924
Amphetamine Distorts Stimulation-Dependent Dopamine Overflow: Effects on D2 Autoreceptors, Transporters, and Synaptic Vesicle Stores
Yvonne Schmitz1, C. Justin Lee2, Claudia Schmauss3, François Gonon4, and David Sulzer1, 3, 4 Departments of 1 Neurology, 2 Physiology and Cellular Biophysics, 3 Psychiatry, Columbia University, 4 and Department of Neuroscience, New York State Psychiatric Institute, New York, New York 10032, and Université Victor Segalen, Bordeaux 33076, France
Amphetamine (AMPH) is known to raise extracellular dopamine (DA) levels by inducing stimulation-independent DA efflux via reverse transport through the DA transporter and by inhibiting DA re-uptake. In contrast, recent studies indicate that AMPH decreases stimulation-dependent vesicular DA release. One candidate mechanism for this effect is the AMPH-mediated redistribution of DA from vesicles to the cytosol. In addition, the inhibition of stimulation-dependent release may occur because of D2 autoreceptor activation by DA that is released via reverse transport. We used the D2 receptor antagonist sulpiride and mice lacking the D2 receptor to address this issue. To evaluate carefully AMPH effects on release and uptake, we recorded stimulated DA overflow in striatal slices by using continuous amperometry and cyclic voltammetry. Recordings were fit by a random walk simulation of DA diffusion, including uptake with Michaelis-Menten kinetics, that provided estimates of DA concentration and uptake parameters. AMPH (10 µM) promoted the overflow of synaptically released DA by decreasing the apparent affinity for DA uptake (Km increase from 0.8 to 32 µM). The amount of DA released per pulse, however, was decreased by 82%. This release inhibition was prevented partly by superfusion with sulpiride (47% inhibition) and was reduced in D2 mutant mice (23% inhibition). When D2 autoreceptor activation was minimal, the combined effects of AMPH on DA release and uptake resulted in an enhanced overflow of exocytically released DA. Such enhancement of stimulation-dependent DA overflow may occur under conditions of low D2 receptor activity or expression, for example as a result of AMPH sensitization.
Key words: dopamine; amphetamine; uptake; amperometry; cyclic voltammetry; D2 receptor; sensitization
Copyright © 2001 Society for Neuroscience 0270-6474/01/21165916-09$05.00/0
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