Introduction

The psychomotor stimulants are distinguished by their drug-abuse liability, their motor effects, and behavioral sensitization. How these effects relate to one another is not clear, but in the past, the studies of these stimulants have centered on dopamine and on the nucleus accumbens and the striatum, two areas of the brain that contain dopaminergic terminal fields, which historically have been implicated in the psychomotor effects of these drugs. The ever more detailed explication of neuroanatomy, specifically of the basal ganglia, makes it obvious that, first, the characteristic actions of the psychomotor stimulants must involve transmitters other than dopamine and brain areas other than the accumbens and the striatum (1-6); second, the effects of the stimulants are mediated by the activation of circuits; third, the different pharmacological properties of the stimulants, such as a motor effect and sensitiza-tion, involve, in part, different circuits, even though they undoubtedly share some neuroeffector systems. Starting with these working hypotheses, we initiated a study some 12 years ago that was designed to identify specific neuroeffectors and discrete brain areas that mediate a stimulant-induced motor effect and behavioral sensitization. The data presented below represent our observations on the general role of dopamine, glutamate, and GABA, as well as their specific functions in the straitum and in the frontal cortex, in enabling stimulant-induced stereotypy and behavioral sensitization.

From the many previous studies that have addressed the question of the relationship among dopamine, glutamate, and GABA function in the striatum and the accumbens, it has become clear that the neuroanatomy of these structures suggests that they interact but not exactly how (7-11); nevertheless, a variety of techniques have been used to allege that both glutamatergic and GABAergic drugs affect the release of dopamine (12). In general, these reports, which include in vivo dialysis studies, have at least two serious flaws in the interpretation of their data. First, very few studies have attempted to quantitatively correlate changes in recovered transmitters with changes in behavior, and, with a few notable exceptions (see, e.g., ref. 13), this includes the in vivo dialysis studies associated with behavioral sensitization. To simply measure recovered transmitters ignores the crucial difference between statistically significant and biologically significant effects, a point that is underscored by the reports that the quantitative behavioral responses do not necessarily parallel the recovered dopamine (for a review, see ref. 14). Such results mandate a consideration of physiological factors other than dopamine in order to understand stimulant-induced behavioral effects, which leads to the proposition that a stimulant effect involves a circuit of interacting transmitter systems and that a functional change in any one of them could quantitatively modify the behavioral response to these drugs.

From: Contemporary Clinical Neuroscience: Glutamate and Addiction Edited by: Barbara H. Herman et al. © Humana Press Inc., Totowa, NJ

Table 1

Qualitative Influence of Systemically Administered Dopamine, Glutamate, and GABA Receptor Antagonists on Amphetamine-Induced Stereotypy in Normal Mice and on the Induction and Expression of Sensitization

Table 1

Qualitative Influence of Systemically Administered Dopamine, Glutamate, and GABA Receptor Antagonists on Amphetamine-Induced Stereotypy in Normal Mice and on the Induction and Expression of Sensitization

Antagonist treatment

Acute

Sensitization Induction

Expression

Dopamine

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