New biological clues linking social connectedness to reduced drug craving and relapse
March 24, 2020
Illustration by Dr. Marco Venniro, NIDA IRP
Research published by Marco Venniro and NIDA colleagues in 2018 found that positive social interaction in rats prevents drug self-administration. When given a choice between interacting with another rat or taking heroin or methamphetamine, the rats consistently chose the social reward.
The researchers also examined the effect of social interaction on incubation of drug craving, a phenomenon in which drug seeking progressively increases after they are no longer given access to drugs—similar to what many human drug users experience during drug abstinence. The researchers provided rats who had been trained to self-administer an addictive drug with a choice between the drug or a rewarding social interaction and found that the rats chose the social reward over the drug. Moreover, the rats who chose to abstain from drugs—as opposed to forced abstinence—were protected against incubation of drug craving.
The current study offers the first mechanistic explanation for the protective effect of social interaction on incubation of craving in rodents, showing that it is mediated by the activation of neurons expressing the enzyme PKCδ in one part of the brain’s amygdala. The scientists also found that activation of a peptide called somatostatin in the amygdala is critical for incubation of drug craving following forced abstinence. In addition, these researchers introduced novel viral tools that will allow other researchers to mechanistically study the role of PKCδ and somatostatin in learned and motivated behaviors related to drug use disorders, as well as other psychiatric disorders.
The rat social choice model used by this team already has clinical implications, with several researchers initiating human studies on brain mechanisms of choice between rewarding social interactions and addictive drugs. Scientists hope that these new findings will stimulate more human research into how social-based treatment approaches might help restore normal amygdala function, resulting in reduced relapse risk.
The research was done by NIDA intramural scientists in collaboration with the Messing lab at the University of Texas in Austin.