Dopamine, the “feel good” brain chemical at the focus of most drug addiction research, helps reinforce drug use. But the negative aspects of drug addiction – e.g., stress-induced relapse – involve other brain systems that may represent therapeutic targets for combating relapse.
Danny Winder, professor of molecular physiology and biophysics, and colleagues are examining the involvement of the adrenergic system and corticotrophin-releasing factor receptor (CRFR) signaling – systems involved in the body’s stress response – in the brain’s response to cocaine. They recorded electrical activity in mouse brain slices and found that activation of beta-adrenergic receptors in the BNST, a region of the amygdala, enhances excitatory neurotransmission through a circuit involving CRFR. Chronic cocaine administration transiently disrupts this enhancement of excitatory neurotransmission. This disruption wanes over time, but can later be recovered by cocaine administration.
The results, published in the June 1 issue of Biological Psychiatry, reveal circuitry within the BNST that may play an important role in drug-seeking behaviors and suggest that this circuitry could provide targets for therapies aimed at preventing relapse.
The research was supported by grants from the National Institute on Alcohol Abuse and Alcoholism and the National Institute on Drug Abuse.
