The National Institutes of Health (NIH) estimates that 50 million people in the United States grapple with the hardships of cocaine or alcohol use disorders.
Besides the well-known health hazards, addiction to these substances also negatively affects cognitive flexibility, our ability to adapt and switch between tasks or strategies.
However, until now, the underlying reasons for this cognitive impairment were largely unknown.
Cognitive flexibility is a critical aspect of various areas in our lives, including academic success, employment stability, and the transition to adulthood.
As we grow older, it also plays an essential role in combating cognitive decline. A deficiency in cognitive flexibility is linked to academic deficits and a reduced quality of life.
A 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, reveals new insights into the damaging impact that chronic substance use has on cognitive flexibility.
Disruption of Inhibitory Brain Circuits
The research, published in the journal Nature Communications, highlights the role of the local inhibitory brain circuit in mediating the adverse effects of substance use on cognitive flexibility.
Substance use affects a specific group of neurons known as striatal direct-pathway medium spiny neurons (dMSNs), with connections to a part of the brain known as the substantia nigra pars reticulata (SNr).
In contrast, cognitive flexibility is facilitated by striatal cholinergic interneurons (CINs), which receive strong inhibitory signals from the striatum.
Dr. Wang’s team hypothesized that increased dMSN activity resulting from substance use inhibits CINs, thereby causing a reduction in cognitive flexibility.
Implications of the Findings
The study confirmed that substance use leads to lasting changes in the inhibitory communication between dMSNs and CINs, dampening cognitive flexibility as a result.
Furthermore, the dMSN-to-SNr brain circuit bolsters drug and alcohol use, while the related collateral dMSN-to-CIN pathway hampers cognitive flexibility.
Dr. Wang summarized the study’s findings: “Our research confirms that substance use induces long-lasting changes in the inhibitory communication between dMSNs and CINs, consequently dampening cognitive flexibility.
Thus, our study provides new insights into the brain circuitry involved in the impairment of cognitive flexibility due to substance use.”
These findings not only improve our understanding of the cognitive effects of substance abuse but could also inform the development of future therapeutic interventions aimed at restoring cognitive function in individuals suffering from substance use disorders.
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The study was published in Nature Communications. Follow us on Twitter for more articles about this topic.
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