Abstract
Collective studies have demonstrated that transcranial ultrasound stimulation (TUS) can elicit activation in hemodynamics, implying its potential in treating cerebral or peripheral vessel-related malfunction. The theory for hemodynamic response to TUS is neurovascular coupling (NVC) following the ultrasound-induced cellular (de)polarization. However, it was not conclusive due to the co-existence of the pathway of direct ultrasound-vessel interactions. This study thus aims to investigate and provide direct evidence for NVC pathway in a rodent model of TUS by inhibiting neural activity with sodium valproate (VPA), a GABAergic agent. Twenty Sprague-Dawley rats were randomly assigned to VPA and Saline groups. Microelectrode and optical imaging were utilized to record local field potential and relative cerebral blood flow (rCBF) during baseline, before, and after TUS periods. We found the attenuated neural activity was associated with reduced rCBF responses. These results provided direct evidence for the presence of NVC pathway in hemodynamic modulation by TUS.
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