Abstract TP93: Ultrasonic Brain Stimulation Regulates Brain Plasticity in Ischemic Mice

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Introduction: Ultrasonic brain stimulation regulates neural activity in different brain regions in normal humans and animals, and promotes neurogenesis in normal mouse brain. However, the role of ultrasonic stimulation in modulating neural plasticity in the ischemic brain is largely unknown.Hypothesis: To explore the effect of ultrasonic brain stimulation on neurological rehabilitation and the possible underlying mechanism.Methods: Adult CD-1 mice (n=18) underwent transient middle cerebral artery occlusion (60 min). One week after brain ischemia, 0.5M HZ frequency brain stimulation was applied transcranially to the ischemic hemisphere of mice for 7 consecutive days. Brain infarct volume and neurological behavioral tests were assessed at 1, 7 and 14 days after brain ischemia. The expression of proteins critical to neuronal development, in particular BrdU and DCX, and IL-10R were examined to explore the underlying mechanism.Results: We found that the brain infarct volume was significantly attenuated in the ultrasonic stimulated mice compared to the non-stimulated mice (p<0.05). Similarly, neurological servility scores, elevated body swing test, and corner test performances were significantly improved in the ultrasonic stimulated mice (p<0.05). Immunohistochemistry results demonstrated that ultrasonic stimulation increased BrdU+/DCX+ cells in the subventricular zone of ischemic mice, suggesting this stimulation promoted neurogenesis in mice after cerebral ischemia. Furthermore, IL-10R expression was substantially up-regulated in the perifocal region and subventricular zone of ischemic mice after ultrasonic stimulation (p<0.05).Conclusions: We concluded that ultrasonic stimulation provided a unique technique to promote neurorehabilitation. Ultrasonic stimulation enhanced neural rehabilitation through promoting neural precursor cell proliferation, which may be modulated by IL-10/IL-10R mediated immune-regulation. (Funded by SJTU YG2016MS62)

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