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Striatal dopamine in bulimia nervosa: A pet imaging study


  • Financial Disclosures: This publication was made possible by NIMH grants R01MH079397, T32MH15144, and K23MH082097; a 2006 NARSAD Junior Investigator Award; and grant number KL2 RR024157 from the National Center for Research Resources (NCRR), a component of the National Institutes of Health (NIH), and NIH Roadmap for Medical Research. Its contents are solely the responsibility of the authors and do not necessarily represent the official view of NCRR or NIH. Information on NCRR is available at Information on Re-engineering the Clinical Research Enterprise can be obtained from search/overview-translational.asp.

  • Dr. Walsh has received research support from AstraZeneca. Dr. Attia has received research support from Eli Lilly. Dr. Abi-Dargham has received support from Bristol-Myers Squibb-Otsuka (as consultant and speaker), Bohringer-Engelheim (as consultant), and GlaxoSmithKline (through research support). Dr. Slifstein has consulted for GlaxoSmithKline and Amgen and has received research support from IntraCellular Therapies and Pierre-Fabre within the past 36 months. The remaining authors (Broft, Shingleton, Kaufman, Liu, Kumar, Schebendach, Van Heertum, and Martinez) report no conflicts.



Bulimia nervosa (BN) has been characterized as similar to an addiction, though the empirical support for this characterization is limited. This study utilized PET imaging to determine whether abnormalities in brain dopamine (DA) similar to those described in substance use disorders occur in BN.


PET imaging with [11C]raclopride, pre/post methylphenidate administration, to assess dopamine type 2 (D2) receptor binding (BPND) and striatal DA release (ΔBPND).


There was a trend toward lower D2 receptor BPND in two striatal subregions in the patient group when compared with the control group. DA release in the putamen in the patient group was significantly reduced and, overall, there was a trend toward a difference in striatal DA release. Striatal DA release was significantly associated with the frequency of binge eating.


These data suggest that BN is characterized by abnormalities in brain DA that resemble, in some ways, those described in addictive disorders. © 2012 by Wiley Periodicals, Inc.