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The Journal of Neuroscience, June 4, 2008, 28(23):5976-5982; doi:10.1523/JNEUROSCI.1153-08.2008

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Behavioral/Systems/Cognitive
Methylphenidate Has Differential Effects on Blood Oxygenation Level-Dependent Signal Related to Cognitive Subprocesses of Reversal Learning

Chris M. Dodds,^1,2 Ulrich Müller,^1,2,3 Luke Clark,^1,2 Anouk van Loon,^1,4 Roshan Cools,^1,5 and Trevor W. Robbins^1,2

¹Behavioral and Clinical Neuroscience Institute and ²Department of Experimental Psychology, University of Cambridge, Cambridge CB2 3EB, United Kingdom, ³Department of Psychiatry, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge CB2 0QQ, United Kingdom, ⁴Department of Psychology, University of Amsterdam, 1018 WB, Amsterdam, The Netherlands, and ⁵F.C. Donders Centre for Cognitive Neuroimaging, Radboud University Nijmegen, 6500 HB, Nijmegen, The Netherlands

Correspondence should be addressed to Chris M. Dodds, Behavioural and Clinical Neuroscience Institute, Department of Experimental Psychology, Downing Street, Cambridge CB2 3EB, UK. Email: cd317{at}cam.ac.uk

Complete understanding of the neural mechanisms by which stimulants such as methylphenidate ameliorate attention deficit hyperactivity disorder is lacking. Theories of catecholamine function predict that the neural effects of stimulant drugs will vary according to task requirements. We used event-related, pharmacological functional magnetic resonance imaging to investigate the effects of 60 mg of methylphenidate, alone and in combination with 400 mg of sulpiride, on blood oxygenation level-dependent (BOLD) signal in a group of 20 healthy participants during probabilistic reversal learning, in a placebo-controlled design. In a whole-brain analysis, methylphenidate attenuated BOLD signal in the ventral striatum during response switching after negative feedback but modulated activity in the prefrontal cortex when subjects maintained their current response set. The results show that the precise neural site of modulation by methylphenidate depends on the nature of the cognitive subprocess recruited.

Key words: methylphenidate; dopamine; striatum; prefrontal cortex; reversal learning; fMRI

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Received Jan. 23, 2008; revised April 23, 2008; accepted April 23, 2008.

Correspondence should be addressed to Chris M. Dodds, Behavioural and Clinical Neuroscience Institute, Department of Experimental Psychology, Downing Street, Cambridge CB2 3EB, UK. Email: cd317{at}cam.ac.uk

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