This study demonstrated that cocaine increases expression of the protein E2F3a in the brain’s reward system. The changes in E2F3a levels in the nucleus accumbens are tied to addiction-related behaviors and to altered gene expression.
This research traced the effects of cocaine-induced disruption of serotonin regulation in the ventral pallidum and orbitofrontal cortex. The findings suggest that these effects may contribute to drug-seeking and cocaine-associated cognitive impairments.
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.
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.
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.
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.
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.
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.
Los investigadores observaron la actividad de dos tipos de neuronas en ratones: las neuronas de "impulso", que promueven los sentimientos de recompensa y la repetición de los comportamientos dirigidos a repetir las experiencias gratificantes, y las neuronas de "control", que disminuyen estos sentimientos e inhiben esos comportamientos.
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.
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.
During investigations into using transcranial brain stimulation (TMS) to treat cocaine abuse, two projects take diverging paths. One researcher moves to the next stage, while another is forced to cut his trial short.
Giving mice a modified version of a naturally occurring gene blocks cocaine’s stimulant effects without affecting the animals’ physiological or metabolic health. The new evidence advances the proposed therapy a step closer to readiness for testing in people.
Two researchers share their reasons for researching transcranial magnetic stimulation (TMS) for treating cocaine addiction, and describe challenges to moving forward this potentially promising therapy.
In mice, a cocaine-induced imbalance in the activity of two key populations of neurons in the reward system persists for a longer period after repeated exposure to the drug. For long-term users, this change could both weaken the cocaine “high” and strengthen the compulsion to seek the drug.
A NIDA-supported study has found that a cocaine-addicted person’s chance of managing 1 whole year of abstinence correlates with activity levels in these impaired motivational and decision-making brain areas.
A can-do attitude, ability to cope with potential triggers for drug use, readiness to change, and participation in self-help programs are major assets for people trying to recover from cocaine addiction.
A stressed rat will seek a dose of cocaine that is too weak to motivate an unstressed rat. Researchers traced the physiological pathway that links stress and the stress hormone corticosterone to increased dopamine activity and heightened responsiveness to cocaine.
Dr. Paul E. M. Phillips spoke on “Phasic Dopamine Transmission During Substance Abuse,” describing investigations that he has led into the role of brief, seconds-long bursts of dopamine signaling in addictive processes. Dr. Rita Z. Goldstein spoke on “Targeting the Brain, Cognition, and Motivation for Intervention in Addiction.”