August 2016 Treatment with an extended-release stimulant medication plus cognitive behavioral therapy was associated with reductions in cocaine use and in attention-deficit/hyperactivity disorder symptoms in patients with both disorders.
Researchers monitored the activity of two types of neurons in mice: “urge” neurons, which promote feelings of reward and repeating behaviors that have produced rewards, and “control” neurons, which dampen those feelings and inhibit behavior.
November 2016 Patients who received transcranial magnetic stimulation (TMS) were more likely to abstain from cocaine than patients who received medications for symptoms associated with abstinence. Researchers concluded that TMS appears to be safe and its efficacy as a treatment for cocaine addiction deserves to be evaluated in a larger clinical trial.
Drugs can alter the way people think, feel, and behave by disrupting neurotransmission, the process of communication between brain cells. This article discusses the central importance of studying drugs’ effects on neurotransmission and describes some of the most common experimental methods used in this research.
Investigators have shown that 2-AG, an endocannabinoid (i.e., a cannabinoid manufactured within the body, as opposed to plant-derived), augments the cocaine-induced dopamine surge in the brain’s reward system.
The discovery adds to evidence that inhibiting activity in the endocannabinoid system might reduce cocaine’s rewarding and addictive effects.
March 2017 In the final installment of this series, Dr. Diana Martinez navigates the process for receiving NIH funding to test the efficacy of using transcranial magnetic stimulation as treatment for cocaine addiction.
September 2017 Electroencephalography (EEG) may provide an objective measure of cocaine-addicted participants’ vulnerability to cue-induced relapse. The assessment of cue-induced responsiveness may be useful in the clinical setting for assessing relapse risk and tailoring interventions to maintain abstinence among cocaine-addicted adults.
Cocaine produces a portion of its rewarding effects by increasing levels of granulocyte-colony stimulating factor (G-CSF) in the brain’s reward center. Treatments that prevent G-CSF signaling in the nucleus accumbens might reduce motivation to use cocaine.