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.
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.”
A can-do attitude, ability to cope with potential triggers for drug use, readiness to change, and participation in self-help programs are major assets for people trying to recover from cocaine addiction.
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.
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.