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.
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.
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.
A meta-analysis of 13 genome-wide association studies of African Americans’ smoking patterns confirms the significance of genetic variation in region 15q25.1. The analysis also tentatively implicates several genome locations that have not previously been associated with smoking behaviors.
New research demonstrated that, in rhesus monkeys, ongoing cocaine exposure weakens two brain functions that people require for successful behavioral change: cognitive flexibility and memory. But the study determined that these changes may not be permanent.