Chen X, Zhang J, and Wang K.
Acta Pharmaceutica Sinica B, 2022.
Research suggests key causative role of TRPV3 in neuronal hyperexcitability and cerebral injury following stroke.
During an ischemic stroke, a lack of blood flow to the brain results in a cascade of metabolic changes and progressive cell death, but these complex interactions are not fully understood. In this study, scientists examined the role of TRPV3 channels in stroke and showed that the overactive intracellular proton-sensitive and calcium-permeable protein plays a key causative role in neuronal hyperexcitability and cerebral injury after stroke—an important finding that may lead to new approaches to the treatment and prevention of ischemic brain injury.
To assess neural network activity label-free and in real time, the scientists used Axion’s in vitro multielectrode array (MEA) platform to examine primary cortical neurons from mice subjected to cerebral ischemic/reperfusion injury and treated with the plant-derived anti-inflammatory TRPV3 inhibitor forsythoside B. Findings from the bioelectronic MEA assays demonstrated that pharmacological inhibition of TRPV3 decreased neuronal firing, burst frequency, and synchrony, and protected against ischemic brain injury. Taken together with results from other testing, the findings suggest that overactive RPV3 channels may lead to more severe neurological deficits in ischemic brain injury but the inhibition of TRPV3 may provide a promising therapeutic avenue for strokes in the future.
