Last updated on January 2019

Brain Dopaminergic Signaling in Opioid Use Disorders

Brief description of study


The chemical messenger dopamine carries signals between brain cells. It may affect addiction. Heavy use of pain medicines called opioids may decrease the amount of dopamine available to the brain. Researchers want to study if decreased dopamine decreases self-control and increases impulsiveness.


To learn more about how opiate use disorder affects dopamine in the brain.


Adults 18-65 years old who are moderate or severe opiate users

Healthy volunteers the same age


Participants will first be screened under another protocol. They will:

  • Have a physical exam
  • Answer questions about their medical, psychiatric, and alcohol and drug use history
  • Take an MRI screening questionnaire
  • Give blood and urine samples
  • Have their breath tested for alcohol

Participants will have up to 3 study visits.

They will have 2-3 positron emission tomography (PET) scans. A radioactive chemical will be injected for the scans. Participants will lie on a bed that slides in and out of the donut-shaped scanner. A cap or plastic mask may be placed on the head.

Vital signs will be taken before and after the PET scans.

Participants will get capsules of placebo or the study drug. They will rate how they feel before, during and after.

Participants will have their breath and urine tested each day.

Participants will have magnetic resonance imaging (MRI) scans. They will lie on a table that slides into a cylinder in a strong magnetic field. They may do tasks on a computer screen while inside the scanner.

Participants will have tests of memory, attention, and thinking.

Participants will wear an activity monitor for one week....

Detailed Study Description

Objectives: Primary objective is to assess whether the balance between dopamine D1 (D1R) and D2 receptors (D2R) signaling in striatum is disrupted in participants with an opioid use disorder (OUD) who are on opioid agonist medication (MAT+: methadone or buprenorphine) relative to OUD participants treated with the opioid antagonist medication (naltrexonel) and OUD participants not being treated with medications (MAT). Secondary objectives are to assess how striatal D1R to D2R availability (assessed with PET) influences: (1) striatal dopamine (DA) release; (2) the function of brain reward and self-control networks (assessed with task fMRI activation and with resting functional connectivity, RFC) and (3) behavior (locomotor activity and neuropsychological tests) and (4) to assess if DA increases, as induced by oral methylphenidate (MP), improve the function of brain reward and control networks in OUD.

Study population: We will complete studies in 120 (n=120) subjects: N=30 healthy control adults and N=90 90 OUD participants (30 MAT+, 30 naltrexone-treated and 30 MAT-) aged 18-65 (male/female) will be included.

Design: Single-blind. Participants will undergo three scans with positron emission tomography (PET): one with [11C]NNC-112 to assess baseline D1R, another with [11C]raclopride after placebo to assess baseline D2R and a third one with [11C]raclopride after MP administration (60mg oral) to assess striatal DA release (assessed as the difference in specific binding of [11C]raclopride between baseline and MP). In addition, participants will undergo two imaging sessions with MRI to assess functional reactivity to drug-cues and to a measure of self-control (delayed discounting task), to assess RFC and to obtain structural brain measures (including diffusion tensor imaging, DTI). One of the sessions will be done under baseline conditions (no drug administered) and the other after MP (about one hour after the [11C]raclopride MP scan is completed). Neuropsychological tests (NP) and accelerometers will be used to assess cognitive performance and locomotor activity respectively

Outcome Measures: Main outcome: (1) Differences in D1R to D2R striatal ratio between participants with an OUD and controls and between MAT+, natrexone, and MAT- groups. Secondary outcomes: Correlations between striatal D1R to D2R and (1) striatal DA release; (2) fMRI activation in reward and controls networks (assessed with cuereactivity and delay discounting tasks, and with RFC) and (3) NP performance and locomotor activity. (4) Differences in fMRI activation and RFC after MP when compared with baseline measures.

Clinical Study Identifier: NCT03190954

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Recruitment Status: Open

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