The second major development in biological approaches to schizophrenia was the demonstration of at least some therapeutic benefit from neu-
roleptics or antipsychotic drugs in treating schizophrenia and the determination that it is positive rather than negative symptoms (see later for this distinction) that respond to these drugs (e.g., Buckley & Meltzer, 1995; Crow, 1980; Weinberger & Lipska, 1995; Wirshing, Marder, Van Putten, & Ames, 1995). The therapeutic efficacy of antipsy-chotic drugs can be attributed to their ability to block DA receptors (e.g., Grace & Moore, 1998; Haracz, 1982; Losonczy, Davidson, & Davis, 1987; Snyder, 1978; Weinberger & Lipska, 1995). This suggests that DA pathways are important in schizophrenia and leads to the dopamine hypothesis of schizophrenia (Snyder, 1978). Much debate has centered on whether an increased sensitivity to dopamine might be a primary etiological factor in schizophrenia. At present, it appears more likely that dopamine makes a secondary contribution by interacting with some other primary deficit that makes the person sensitive to dopaminergic activity (e.g., Healy, 1989; Liddle, Carpenter, & Crow, 1993; Weinberger & Lipska, 1995).
Regardless of the eventual explanation, these findings concerning DA must be incorporated into a theory of schizophrenia. To bridge the theoretical gulf between neuroregulator effects and behavior, two questions must be answered: What are the behavioral implications of activity in the DA pathways? What do DA-related behaviors have to do with the behavioral phenomena of schizophrenia? If it is true that the mesolimbic (and mesocortical) DA pathways are involved in the BAS (activation of behavior in response to cues for reward and relieving nonpunishment with an accompanying positive hedonic tone), it is likely that antipsychotic drugs reduce activity in this system. From this perspective, one of the major behavioral effects of these drugs would be to reduce the responsiveness of the BAS. As expected from this hypothesis, patients treated with antipsy-chotic drugs show reduced positive affect and reduced sensitivity to rewards—that is, pharmacologically induced anhedonia (Harrow, Yonan, Sands, & Marengo, 1994; Healy, 1989; Sommers, 1985) that involves a range of negative symptoms (e.g., lack of emotional reactivity, lack of goal-directedness, reduced or retarded speech, diminished social and vocational initiative, etc.).
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