Prenatal drug exposure can have behavioral effects that last well into adulthood, according to two studies of adult monkeys prenatally exposed to cocaine. In the first study, drug-exposed monkeys exhibited less flexibility than controls in adjusting to changing circumstances; in the second study, drug-exposed males exhibited a greater preference than controls for having rewards right away, a sign of impulsivity.
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 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.
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.