Pathophysiological and behavioral deficits in developing mice following rotational acceleration-deceleration traumatic brain injury

摘要: ABSTRACT Abusive head trauma (AHT) is the leading cause of death from in infants and young children. An AHT animal model was developed on 12-day-old mice subjected to 90° extension-flexion sagittal shaking repeated 30, 60, 80 100 times. The mortality time until return consciousness were dependent number repeats severity injury. Following 60 episodes shakings, pups demonstrated apnea and/or bradycardia immediately after Acute oxygen desaturation observed by pulse oximetry during respiratory cardiac suppression. cerebral blood perfusion assessed laser speckle contrast analysis (LASCA) using a PeriCam PSI system. There severe reduction that did not significantly improve within 24 h. injured began experience reversible sensorimotor function at 9 days postinjury (dpi), which had completely recovered 28 dpi. However, cognitive deficits anxiety-like behavior remained. Subdural/subarachnoid hemorrhage, damage brain-blood barrier parenchymal edema found all insults. Proinflammatory response reactive gliosis upregulated 3 dpi. Degenerated neurons cortex olfactory tubercles 30 dpi. This mouse repetitive brain injury rotational acceleration-deceleration partially mimics major pathophysiological behavioral events occur children with AHT. resultant hypoxia/ischemia suggests potential mechanism underlying secondary acceleration-deceleration-induced developing mice.