First Advisor

Miranda M. Lim

Date of Award


Document Type


Degree Name

Bachelor of Science (B.S.) in Biology and University Honors




Sleep deprivation -- Physiological aspects, Dendrites, Prefrontal cortex, Prairie vole, Developmental neurophysiology, Rapid eye movement sleep




Synaptic pruning within neurons in the brain during development allows for maintenance of proper neuronal connections and the elimination of aberrant ones. Rapid eye movement (REM) sleep is critical for pruning and maintaining new synapses formed during both development and learning. We hypothesize that disrupting REM sleep early in life will result in long lasting changes in synaptic density in cortical brain regions. The prefrontal cortex (PFC) is a late-maturing region that modulates higher order social and cognitive functions. Abnormally high dendritic spine density in the PFC is implicated in neurodevelopmental disorders such as autism spectrum disorder (ASD). Emerging research in our lab suggests that selectively suppressing REM sleep early in life in the socially monogamous prairie vole (Microtus ochrogaster) impairs social development and increases inhibitory interneurons in the PFC, consistent with ASD pathology. Using Golgi-Cox staining in adult prairie vole post-mortem tissue, we quantified dendritic spines in the prefrontal cortex in adult animals that underwent early life sleep disruption (ELSD). In males, ELSD increased spine density and decreased spine width selectively in the apical oblique distal (> 90 µm) segments of pyramidal neurons in prelimbic cortex layers II/III. Distal dendrites reflect long range inputs from further cortical and thalamic regions, suggesting that ELSD may lead to an impaired ability to integrate sensory information. Ongoing work will examine dendritic spine density and morphology earlier in development and in additional brain regions, including the primary somatosensory cortex and other layers of the PFC. Results from these studies will enhance our understanding of how modulation of sleep early in life contributes to the neuropathology of developmental disorders.


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