Selective Corticostriatal Dysfunction in Schizophrenia: Examination of Motor and Cognitive Skill Learning Karin Foerde, Russell A. Poldrack, and Barbara J. Knowlton University of California Los Angeles Fred W. Sabb, Susan Y. Bookheimer, Robert M. Bilder, and Don Guthrie David Geffen School of Medicine at University of California Los Angeles Eric Granholm University of California San Diego and VA San Diego Healthcare System Keith H. Nuechterlein David Geffen School of Medicine at University of California Los Angeles Stephen R. Marder University of California Los Angeles Neuropsychiatric Institute, and West Los Angeles VA Robert F. Asarnow David Geffen School of Medicine at University of California Los Angeles It has been suggested that patients with schizophrenia have corticostriatal circuit dysfunction (Carlsson & Carlsson, 1990). Skill learning is thought to rely on corticostriatal circuitry and different types of skill learning may be related to separable corticostriatal loops (Grafton, Hazeltine, & Ivry, 1995; Poldrack, Prabhakaran, Seger, & Gabrieli, 1999). The authors examined motor (Serial Reaction Time task, SRT) and cognitive (Probabilistic Classification task, PCT) skill learning in patients with schizophrenia and normal controls. Development of automaticity was examined, using a dual task paradigm, across three training sessions. Patients with schizophrenia were impaired at learning on the PCT compared to controls. Performance gains of controls occurred within the first session, whereas patients only improved gradually and never reached the performance level of controls. In contrast, patients were not impaired at learning on the SRT relative to controls, suggesting that patients with schizophrenia may have dysfunction in a specific corticostriatal subcircuit. Keywords: schizophrenia, corticostriatal circuits, skill learning, automaticity, Supplemental material: http://dx.doi.org/1037/0894-4105.22.1.100.supp There is a longstanding hypothesis that the pathophysiology of schizophrenia is related to dysfunction of corticostriatal circuits (e.g., Kleist, 1960). There are structural abnormalities in the basal ganglia in patients with schizophrenia (Buchsbaum, 1990) as well as neurochemical imbalances in the corticostriatal circuits (Carls- son & Carlsson, 1990). In addition, corticostriatal dysfunction can account for some key neuropsychological deficits, such as im- paired volition and planning, found in patients with schizophrenia (Frith, 1987; Robbins, 1990; Pantelis et al., 1997). However, corticostriatal circuits have been relatively understudied in schizo- phrenia, particularly in comparison to the extensive literature on frontal and temporal functions. Corticostriatal circuitry is characterized by several anatomically and functionally discrete loops (Alexander, DeLong, & Strick, 1986; Lehericy et al., 2004). Frontal lobe regions project to distinct regions of the neostriatum, from the neostriatum neurons project to the globus pallidus (GP), from the GP to the thalamus, and from the thalamus back to frontal regions. The same general architecture Karin Foerde, Department of Psychology, UCLA; Russell A. Poldrack, Department of Psychology, UCLA; Barbara J. Knowlton, Department of Psychology, UCLA; Fred W. Sabb, Department of Psychiatry, David Geffen School of Medicine at UCLA; Susan Y. Bookheimer, Department of Psychiatry, David Geffen School of Medicine at UCLA; Robert M. Bilder, Department of Psychiatry, David Geffen School of Medicine at UCLA; Don Guthrie, Department of Psychiatry, David Geffen School of Medicine at UCLA; Eric Granholm, Department of Psychiatry, UCSD and VA San Diego Healthcare System; Keith H. Nuechterlein, Department of Psychol- ogy, UCLA and Department of Psychiatry, David Geffen School of Medicine at UCLA; Stephen R. Marder, UCLA Neuropsychiatric Institute, and West Los Angeles VA; Robert F. Asarnow, Department of Psychology, UCLA and Department of Psychiatry, David Geffen School of Medicine at UCLA. We thank the patients who participated in this study. We thank Marie Luna, Brittany Scott, and Vindia Fernandez for help with data collection. This work was supported by the Della Martin Foundation, a National Science Foundation Graduate Fellowship to KF, and a National Institute of Mental Health grant (MH 72697). We also acknowledge National Institute of Mental Health Grants MH 66286 and MH 37705, NIH Roadmap Initiative Grant RR020750, and the VA Desert-Pacific Mental Illness Research, Education, and Clinical Center. Correspondence concerning this article should be addressed to Karin Foerde, Department of Psychology, Columbia University, 1190 Am- sterdam Avenue, MC 5501, New York, NY 10027. E-mail: kf2265@ columbia.edu CORRECTED JANUARY 24, 2008; SEE LAST PAGE Neuropsychology Copyright 2008 by the American Psychological Association 2008, Vol. 22, No. 1, 100 –109 0894-4105/08/$12.00 DOI: 10.1037/0894-4105.22.1.100 100