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.
NIDA-supported research suggests that glucocorticoid receptor levels during early brain development affect the hard wiring of neural circuits that shape an individual’s basic emotional makeup. In mice, overexpression of the glucocorticoid gene in the first weeks after birth increased anxiety and response to cocaine in adulthood. These findings may help researchers understand the genetic background and the developmental trajectory of 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.
Individuals with weak signaling in a nicotine-sensitive brain circuit were more vulnerable to nicotine dependence than those with stronger signaling, according to a study conducted while the subjects’ brains were in a resting state. A second resting-state study finds that the same circuit appears to mediate dependence associated with a genetic risk factor for smoking.
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.