Early life sleep shapes brain development and social behavior in the socially monogamous prairie vole
Description
Miranda M. Lim, MD, PhD
Dr. Miranda Lim is board-certified in Neurology and Sleep Medicine and is Professor in the Department of Neurology at Oregon Health & Science University. As a physician-scientist, Dr. Lim leads a comprehensive basic, translational, and clinical research program called Sleep & Health Applied Research Program (SHARP).
Dr. Lim completed a combined MD/PhD degree from Emory University School of Medicine, followed by a neurology residency at Washington University in Saint Louis, and fellowship in Sleep Medicine at University of Pennsylvania. Dr. Lim has numerous scientific publications in high impact journals including Nature, Science, Journal of Clinical Investigation, Science Advances, SLEEP, and Science Translational Medicine. Early in her career, Dr. Lim received the United States Presidential Early Career Award for Scientists and Engineers (PECASE), the highest honor bestowed by the United States federal government on outstanding scientists and engineers. The SHARP research program, with support from the federal agencies NIH, DoD, VA, NSF and private foundations, examines the mechanisms by which sleep promotes brain health, and sleep’s critical interface with neurological disorders such as autism spectrum disorder, Alzheimer’s, Parkinson’s, and traumatic brain injury (TBI).
Lab website: https://www.sharplabpdx.com/
Description: Sleep is important for brain development, and disrupted sleep early in life is common in developmental disorders, such as autism spectrum disorder. Individuals with autism have difficulty engaging in complex social behaviors. By studying the wild prairie vole, a highly social monogamous rodent, Dr. Lim's team has shown that early life sleep disruption during a sensitive developmental window affects brain circuitry and impairs social bonding between voles. Impaired social bonding was associated with changes in dendritic spine density in the prefrontal cortex (widely regarded as a marker of excitatory inputs), and parvalbumin-expressing GABAergic interneurons within the primary somatosensory barrel cortex (a marker of inhibition), both areas implicated in human autism and associated sensory processing disorders. Thus, these data advance the idea that the function of early life sleep may be to provide proper tuning of social circuits in the brain, and that sleep may be a modifiable risk factor in the pathogenesis of autism spectrum disorder.
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