Chronic use of cocaine or alcohol impairs cognitive flexibility, with a recent study revealing the role of inhibitory brain circuits in this impairment. The research found that substance use alters neuron activity, dampening cognitive flexibility, and sheds light on potential therapeutic interventions for substance-induced cognitive decline.
Research from Texas A&M underlines the link between substance use and significant changes in an inhibitory brain circuit, leading to reduced cognitive flexibility.
According to the National Institutes of Health (NIH), approximately 50 million people in the United States are grappling with the difficulties posed by alcohol or cocaine use disorders. These addictions not only pose significant health dangers, which are well chronicled but also impair our cognitive flexibility, which is the ability to adapt and switch between different tasks or strategies. While past studies have suggested a link between substance addiction and this form of cognitive decline, the underlying reasons for this cognitive impairment remain elusive.
Cognitive flexibility is a crucial element in various domains of our lives, including academic achievement, employment success, and transitioning into adulthood. As we age, this flexibility plays an important role in mitigating cognitive decline. A deficiency in cognitive flexibility, however, is linked to academic deficits and a lower quality of life.
A groundbreaking study led by Dr. Jun Wang, associate professor in the Department of Neuroscience and Experimental Therapeutics at the Texas A&M University School of Medicine, provides new insight into the damaging impact that chronic cocaine or alcohol use has on cognitive flexibility. The research, published in the journal Nature Communication, emphasizes the role of the local inhibitory brain circuit in mediating the negative effects of substance use on cognitive flexibility.
Substance use influences a specific group of neurons called striatal direct-pathway medium spiny neurons (dMSNs), with projections to a part of the brain known as the substantia nigra pars reticulata (SNr). Conversely, cognitive flexibility is facilitated by striatal cholinergic interneurons (CINs), which receive potent inhibitory signals from the striatum.
“Our hypothesis was that increased dMSN activity from substance use inhibits CINs, leading to a reduction in cognitive flexibility,” Wang said. “Our research confirms that substance use induces long-lasting changes in the inhibitory communication between dMSNs and CINs, consequently dampening cognitive flexibility. Furthermore, the dMSN-to-SNr brain circuit reinforces drug and alcohol use, while the associated collateral dMSN-to-CIN pathway hinders cognitive flexibility. Thus, our study provides new insights into the brain circuitry involved in the impairment of cognitive flexibility due to substance use.”
Wang and his team are optimistic about the potential therapeutic applications of their findings and anticipate that they could inform new treatment strategies for substance-induced cognitive decline. The research receives support from the National Institute on Alcohol Abuse and Alcoholism (NIAAA) and an X-grant from the Presidential Excellence Fund at Texas A&M University.
Reference: “Drug reinforcement impairs cognitive flexibility by inhibiting striatal cholinergic neurons” by Himanshu Gangal, Xueyi Xie, Zhenbo Huang, Yifeng Cheng, Xuehua Wang, Jiayi Lu, Xiaowen Zhuang, Amanda Essoh, Yufei Huang, Ruifeng Chen, Laura N. Smith, Rachel J. Smith and Jun Wang, 30 June 2023, Nature Communications.
DOI: 10.1038/s41467-023-39623-x
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