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.
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.
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.
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.