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Monoamine Contributions to Neurocircuitry in Eating Disorders

This study has been completed.
National Institute of Mental Health (NIMH)
Information provided by (Responsible Party):
Walter Kaye, University of California, San Diego Identifier:
First received: December 11, 2013
Last updated: May 17, 2016
Last verified: May 2016
This study will use brain imaging technologies to measure several neurotransmitters (serotonin and dopamine) that contribute to our abilities to respond to reward or inhibit our impulses, and which are known to be altered in the brain of people with anorexia nervosa (AN) and bulimia nervosa (BN). Because palatable food stimulates dopamine secretion, we propose to use a challenge with brain imaging that will stimulate dopamine release which we hypothesize will generate anxiety rather than pleasure in AN, and will help explain why AN restrict eating in order to reduce anxiety. This study will help to understand the unique puzzling symptoms in eating disorders and contribute to finding better methods for identifying effective treatments for these often relapsing and sometimes chronic disorders.

Condition Intervention Phase
Eating Disorder
Drug: [11C]raclopride
Drug: [11C]DASB
Drug: amphetamine
Phase 4

Study Type: Interventional
Study Design: Intervention Model: Single Group Assignment
Masking: Open Label
Primary Purpose: Basic Science
Official Title: Monoamine Contributions to Neurocircuitry in Eating Disorders

Resource links provided by NLM:

Further study details as provided by University of California, San Diego:

Primary Outcome Measures:
  • 1. 5-HT transporter binding and Dopamine (DA) D2/D3 binding as measured during the PET scan [ Time Frame: 90 minute PET scan ]
    Use PET and [11C]DASB and [11C]raclopride to explore 5-HTT and DA D2/D3 receptor binding potential in cortical, subcortical and striatal ROIs.

Secondary Outcome Measures:
  • Change in [11C]raclopride binding potential from baseline to post-amphetamine administration as measured during the two 90 min PET scans. [ Time Frame: Two 90 min PET scans ]
    The change (Δ) in BPND (the difference between the [11C]raclopride BPND at baseline and post-AMPH treatment normalized to the baseline BPND).

Enrollment: 88
Study Start Date: May 2011
Study Completion Date: April 2016
Primary Completion Date: April 2016 (Final data collection date for primary outcome measure)
Arms Assigned Interventions
Experimental: [11C]raclopride, [11C]DASB, amphetamine
One time administration of oral amphetamine based on subject's weight (0.5 mg/kg). One PET scan using [11C]DASB. Two PET scans using [11C]raclopride.
Drug: [11C]raclopride
1.[11C]raclopride -The change (Δ) in BPND (the difference between the [11C]raclopride BPND at baseline and post-AMPH treatment normalized to the baseline BPND
Other Name: Raclopride, serial number 009
Drug: [11C]DASB
BPND of [11C]DASB.
Other Name: DASB, serial number 0011
Drug: amphetamine
The change (Δ) in BPND (the difference between the [11C]raclopride BPND at baseline and post-AMPH treatment normalized to the baseline BPND.
Other Name: dextroamphetamine

Detailed Description:
Alterations of serotonin (5-HT) and dopamine (DA) activity may contribute to extremes of appetitive behaviours in anorexia nervosa (AN) and bulimia nervosa (BN), through effects on inhibitory and reward neural pathways. To avoid the confounding effects of malnutrition, and because they have behaviours and neural circuit alterations relevant for this study, we will study 25 recovered (REC) restricting-type AN, 25 REC bulimic-type AN (AN-BN), 25 REC BN, and 25 control women (CW). This 5 year study, of women 18 to 45 years old, will employ positron emission tomography (PET) imaging with radioligands for the 5-HT transporter ([11C]DASB) and DA D2/D3 receptors ([11C]raclopride).

Ages Eligible for Study:   18 Years to 45 Years   (Adult)
Sexes Eligible for Study:   Female
Accepts Healthy Volunteers:   Yes


  • history of DSM-IV diagnosis of anorexia or bulimia.
  • AN women have history of ABW below 85% for height.
  • AN-BN subjects have history of ABW below 85% ABW.
  • AN-BN subjects have history of binging/purging behaviors during a period of low weight.
  • Subjects must be right-handed.
  • Subjects have been recovered for 12 months or more.


  • Diagnosis of alcohol or drug abuse or dependence in the 3 months.
  • Alcohol or substance use within 30 days.
  • Current diagnosis of an Axis I disorder.
  • Organic brain syndromes, dementia, psychotic disorders, or mental retardation.
  • Neurological or medical disorders such as seizure disorder, renal disease, diabetes, thyroid disease, EKG indicative of electrolyte imbalance
  • BN subjects whose purging methods were the use of laxatives, diuretics
  • Use of psychoactive medication in the 3 months.
  • Pregnancy or lactation.
  • Tobacco use in the 3 months.
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Please refer to this study by its identifier: NCT02020408

United States, California
University of California San Diego
San Diego, California, United States, 92102
Sponsors and Collaborators
University of California, San Diego
National Institute of Mental Health (NIMH)
Principal Investigator: Walter Kaye, MD UCSD
  More Information

Responsible Party: Walter Kaye, MD, University of California, San Diego Identifier: NCT02020408     History of Changes
Other Study ID Numbers: 090661
R01MH092793 ( US NIH Grant/Contract Award Number )
Study First Received: December 11, 2013
Last Updated: May 17, 2016

Additional relevant MeSH terms:
Feeding and Eating Disorders
Pathologic Processes
Mental Disorders
Central Nervous System Stimulants
Physiological Effects of Drugs
Autonomic Agents
Peripheral Nervous System Agents
Dopamine Agents
Neurotransmitter Agents
Molecular Mechanisms of Pharmacological Action
Adrenergic Agents
Adrenergic Uptake Inhibitors
Neurotransmitter Uptake Inhibitors
Membrane Transport Modulators
Dopamine Uptake Inhibitors
Antipsychotic Agents
Tranquilizing Agents
Central Nervous System Depressants
Psychotropic Drugs
Dopamine Antagonists processed this record on May 22, 2017