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.
Some teens' marijuana use has been linked to disrupted communication between two key regions in the brain’s reward circuitry at age 20. Disrupted communication between the regions was associated with poorer psychosocial functioning at age 22.
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.
Las drogas pueden alterar la manera de pensar, sentir y comportarse de las personas al afectar la neurotransmisión, que es el proceso que usan las neuronas (células nerviosas) en el cerebro para comunicarse entre ellas. Este artículo trata sobre la importancia central de estudiar los efectos de las drogas sobre la neurotransmisión y describe algunos de los métodos experimentales más comunes que se usan en esta investigación. Lea este artículo en inglés.
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.
New studies show that two novel compounds powerfully suppressed animals’ pain responses, while producing little or none of the respiratory depression and liability for misuse and abuse associated with morphine and other typical opioids.
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.
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.
A new study proposes that research into the discrete roles played by the brain’s two hemispheres could yield important and actionable insights into drug use and addiction. Evidence indicates that two risk factors for substance use, impulsivity and craving, primarily reflect activity in the right and left hemispheres, respectively.
A brain imaging study strongly suggests that regular users of marijuana have smaller orbitofrontal cortex (OFC) volumes. Such a deficit could make it more difficult to change counterproductive behaviors, including drug use.
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.
Young adults who had been maltreated as children differed from others who had not been maltreated in the connectivity of nine cortical regions. The differences could compromise the maltreated group’s basic social perceptual skills, ability to maintain a healthy balance between introversion and extroversion, and ability to self-regulate their emotions and behavior.
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 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.
Can marijuana use put offspring at heightened risk for opiate addiction, even if the use stops before the offspring are conceived? Results from a recent NIDA-funded study are consistent with other studies suggesting that a parent’s history of drug use, even preconception, may affect a child’s brain function and behavior.
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.”
The Scientific Director of NIDA’s Intramural Research Program talks about switching off animals’ compulsive cocaine seeking by optogenetically activating the prefrontal cortex, and the implications of this work for people. In an accompanying podcast, Dr. Bonci walks viewers through experiments that showed that prefrontal cortex activity levels may constitute a simple switch controlling whether or not animals compulsively seek cocaine.
Two recent studies suggest that genotyping may enable clinicians to base therapies on individual patients’ potential responsiveness to opioid drugs’ therapeutic effects and vulnerability to their harmful effects.
A brain response occurs in the nucleus accumbens when rats encounter a cue that they associate with previous cocaine self-administration, but not a cue associated with a pleasurable non-drug experience. Moreover, the response correlates in time and intensity with the animals’ cue-induced relapse to cocaine-seeking.
One of NIDA’s goals is to try to understand the individual differences that contribute to whether or not someone who takes a drug will become addicted to it. Dr. Rutter’s research focuses on three types of differences: Environmental, developmental, and genetic and epigenetic.
Methamphetamine alters brain structures involved in decision-making and impairs the ability to suppress habitual behaviors that have become useless or counterproductive. The two effects were correlated, indicating that the structural change underlies the decline in mental flexibility.
Ketoprofen, an anti-inflammatory agent commonly prescribed to treat arthritis, reduces neuronal damage in rats that have been exposed to chronic stress and methamphetamine. If this finding of a recent NIDA-supported study extrapolates to humans, anti-inflammatory medications may gain a place in the treatment of methamphetamine addiction.
Researchers have shut down laboratory rats’ compulsive cocaine seeking by stimulating an area of the animals’ prefrontal cortex. The finding raises the possibility that stimulating neurons in this brain area may weaken or break cocaine’s grip on the behavior of people who are addicted to the drug.