The dopamine D3 receptor antagonist VK4-116 reduced oxycodone self-administration in rats, as well as drug-seeking behaviors after oxycodone reinstatement following withdrawal. VK4-116 did not interfere with oxycodone’s pain-relieving effects
In animal studies, α2δ-1 and its interactions with NMDA receptors in the spinal cord triggered the pain sensitivity and analgesic tolerance that occurs with chronic morphine treatment. Blocking the α2δ-1–NMDA interaction reduced opioid-induced hyperalgesia and analgesic tolerance.
This study showed that rats will forgo heroin and methamphetamine in favor of spending time with another rat. It also highlights the importance of incorporating voluntary choice between drugs and social rewards in drug addiction research.
Exposing adolescent rats to THC disrupted normal maturation of a key set of neurons in a brain area that corresponds to the human prefrontal cortex. The disruptions produced structural differences that resemble patterns which have been observed in people with addiction and schizophrenia.
These findings add to research showing that nicotine and cannabis have interactive effects on brain structure and function. They also suggest that specialized treatment interventions may be appropriate for people who use both drugs.
People with cannabis dependence have changes in neural circuitry in brain regions related to reward processing, habit formation, and psychopathology. These changes in neural circuitry may provide a useful marker for tracking psychopathology associated with cannabis misuse.
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.
La presente investigación: arroja luz sobre un mecanismo clave del desarrollo del cerebro adolescente; demuestra de qué manera las anfetaminas alteran ese mecanismo; establece un vínculo entre esa alteración y las conductas observadas en animales, similares a la susceptibilidad del ser humano a la adicción.
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.
Los investigadores patrocinados por el NIDA mostraron que, en los monos, la metanfetamina altera las estructuras cerebrales involucradas en la toma de decisiones y afecta negativamente la capacidad de eliminar los comportamientos habituales que se han vuelto inútiles o contraproducentes.
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.