According to the National Institutes of Health (NIH), approximately 50 million individuals in the United States struggle with cocaine or alcohol use disorders. These addictions not only pose significant health risks but also have a detrimental impact on cognitive flexibility, which refers to our ability to adapt and switch between tasks or strategies. While previous research has suggested a link between substance use and cognitive impairment, the underlying reasons behind this connection have remained elusive.
Cognitive flexibility plays a crucial role in various aspects of life, including academic achievement, employment success, and transitioning into adulthood. As we age, cognitive flexibility becomes even more important in mitigating cognitive decline. However, a deficiency in cognitive flexibility is associated with academic deficits and a lower quality of life.
A recent study led by Dr. Jun Wang, an associate professor in the Department of Neuroscience and Experimental Therapeutics at the Texas A&M University School of Medicine, sheds new light on the damaging effects of chronic cocaine or alcohol use on cognitive flexibility.
Published in the journal Nature Communications, the research highlights the role of a local inhibitory brain circuit in mediating the negative effects of substance use on cognitive flexibility.
Substance use affects a specific group of neurons called striatal direct-pathway medium spiny neurons (dMSNs), which project to a region of the brain called the substantia nigra pars reticulata (SNr). On the other hand, cognitive flexibility is facilitated by striatal cholinergic interneurons (CINs), which receive strong inhibitory signals from the striatum.
“Our hypothesis was that increased dMSN activity resulting from substance use inhibits CINs, leading to a reduction in cognitive flexibility,” explains Wang.
“Our research confirms that substance use causes long-lasting changes in the inhibitory communication between dMSNs and CINs, ultimately dampening cognitive flexibility. Furthermore, the brain circuitry from dMSNs to SNr reinforces drug and alcohol use, while the associated collateral pathway from dMSNs to CINs hinders cognitive flexibility. Thus, our study provides new insights into the brain circuitry involved in the impairment of cognitive flexibility due to substance use.”
Source: Texas A&M University