Poster abstracts
Poster number 97 submitted by Samuel Houle
Post injury sleep fragmentation stress increases neuroinflammatory response and impairs behavioral recovery
Sam Houle (Department of Neuroscience, Institute for Behavioral Medicine Research), Zoe Tapp (Department of Neuroscience, Institute for Behavioral Medicine Research), Zachary Zimomra (Department of Neuroscience), Christopher Cotter (Department of Neuroscience, Institute for Behavioral Medicine Research), Sakeef Ahsan (Department of Neuroscience), Shannon Dobres (Department of Neuroscience)
Abstract:
Traumatic brain injury (TBI) causes neuroinflammation driven by microglia. In TBI survivors, environmental sleep fragmentation (SF) elicits a stress response. We hypothesized that SF-induced stress would exaggerate and prolong neuroinflammation, impairing recovery in a maurine model of TBI. Here, we investigated the effects of daily, SF by mechanical disturbance from 5am-10am (L:D 6-6) following lateral fluid percussion injury or sham injury. At 14 days post-injury (DPI), SF ended, and mice recovered until 30DPI. Outcome measures included sleep/wake behavior (1-30 DPI), cognitive function (7, 14, 27 DPI), and cortical gene expression changes (14, 30 DPI).
SF increased percent sleep and altered regulation of sleep bouts observed during the dark period. Sham-SF mice engaged in more sleep bouts and slept higher percentages of each hour than sham controls during the dark period from 8-14 DPI. Similar changes were not observed between TBI-SF and TBI controls. Additionally, SF interacted with TBI to increase escape latency from the Morris water maze 14 DPI. Transcriptional profiles of glial-related genes from 14 and 30 DPI showed that stress impaired the brain’s normal recovery from TBI and conveyed long-lasting impacts on neuroimmune function. Interestingly, SF suppressed neurogenesis-related genes and canonical pathways at 14 DPI while exaggerating complement and oxidative stress pathways at 30 DPI. Microglial related genes associated with Alzheimer’s disease were significantly increased by post-TBI SF 14 and 30 DPI. Together, these data indicate that post-TBI stress delays recovery from TBI and may convey chronic impairments. Therefore, reducing stress exposure may be instrumental in TBI recovery.
Keywords: Neurotrauma, Sleep, Inflammation