The National Institutes of Health (NIH) estimates that 50 million people in the United States struggle with cocaine or alcohol use disorders. Beyond the factual wellbeing chances, dependence on these substances unfavorably influences our mental adaptability, which is the capacity to adjust and switch between various undertakings or procedures. Although past examinations have alluded to this association, the fundamental explanations behind this mental disability remain tricky.
Cognitive flexibility is important for many aspects of our lives, like getting good grades, finding work, and becoming an adult. This adaptability helps prevent cognitive decline as we get older. A lack of mental adaptability, nonetheless, is connected to scholastic shortages and lower personal satisfaction.
Dr. Jun Wang, an associate professor in the Texas A&M University School of Medicine’s Department of Neuroscience and Experimental Therapeutics, led a study that sheds new light on the detrimental effects of long-term cocaine or alcohol use on cognitive flexibility.
“Our hypothesis was that increased dMSN activity from substance use inhibits CINs, resulting in a decrease in cognitive flexibility,”
Dr. Jun Wang, associate professor in the Department of Neuroscience and Experimental Therapeutics.
The study, which was published in Nature Communications, focuses on how the local inhibitory brain circuit mediates the detrimental effects of substance use on cognitive flexibility.
Substance utilizes the power of a particular gathering of neurons called striatal direct-pathway medium prickly neurons (dMSNs), with projections to a piece of the mind known as the substantia nigra standards reticulata (SNr). In contrast, striatal cholinergic interneurons (CINs), which receive potent inhibitory signals from the striatum, facilitate cognitive flexibility.
Wang stated, “Our hypothesis was that substance use causes increased dMSN activity that inhibits CINs, leading to a reduction in cognitive flexibility.”
“Our examination affirms that substance use actuates enduring changes in the inhibitory correspondence among dMSNs and CINs, thus hosing mental adaptability. Additionally, the associated collateral dMSN-to-CIN pathway restricts cognitive flexibility, while the dMSN-to-SNr brain circuit encourages drug and alcohol use. As a result, our research sheds new light on the brain circuitry that contributes to substance abuse-related cognitive flexibility impairment.”
More information: Himanshu Gangal et al, Drug reinforcement impairs cognitive flexibility by inhibiting striatal cholinergic neurons, Nature Communications (2023). DOI: 10.1038/s41467-023-39623-x
