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Using the Activity-based Anorexia Rodent Model to Study the Neurobiological Basis of Anorexia Nervosa
Published on: October 22, 2015
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Striatal dopamine type 2 receptor availability in anorexia nervosa
Allegra Broft1, Mark Slifstein1, Joseph Osborne2
1Columbia University Medical Center/New York State Psychiatric Institute, Department of Psychiatry, 1051 Riverside Drive, New York, NY, USA.
Psychiatry Research
|August 15, 2015
Summary
Neuroimaging reveals no differences in striatal dopamine D2 receptor availability in patients with anorexia nervosa compared to controls. Weight restoration did not alter these dopamine receptor levels, suggesting other neural mechanisms are involved in reward processing.
Area of Science:
- Neuroscience
- Psychiatry
- Radiology
Background:
- The neurobiology of anorexia nervosa (AN) is not fully understood.
- Reward system dysregulation is implicated in AN.
- Dopamine type 2 (D2) receptors are key in reward processing.
Purpose of the Study:
- To measure striatal dopamine D2 receptor availability in women with AN.
- To compare D2 receptor availability between AN patients and healthy controls.
- To assess changes in D2 receptor availability after weight restoration in AN patients.
Main Methods:
- Positron Emission Tomography (PET) imaging was used.
- The radiotracer [(11)C]raclopride was employed to quantify D2 receptor binding potential.
- 25 women with AN and 25 control subjects were recruited.
Main Results:
- No significant differences in striatal D2 receptor binding potential were found between underweight AN patients and controls.
- Subregional analyses of the striatum (sensorimotor, associative, limbic) also showed no group differences.
- No significant changes in D2 receptor binding potential were observed after weight restoration in AN patients.
Conclusions:
- Striatal D2 receptor availability does not appear to be altered in anorexia nervosa.
- Weight restoration does not normalize striatal D2 receptor binding.
- Reward processing disturbances in AN may involve other neural targets beyond D2 receptors.
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