![]() Thus, our study proposes a novel mechanism: hyperthermia activates TRPV4 and induces brain edema after ischemia. Finally, we found that brain edema following traumatic brain injury was suppressed in TRPV4-deficient male mice in vivo. Furthermore, using the temperature-dependent fluorescence lifetime of a fluorescent-thermosensitive probe, we confirmed that OGD treatment increases the temperature of brain slices through the activation of glutamate receptors. ![]() Because TRPV4 is activated at around body temperature and its activation is enhanced by heating, we next elevated the temperature of the perfusate in the recording chamber, finding that hyperthermia induces swelling via TRPV4 activation. OGD-induced swelling was prevented by pharmacologically blocking or genetically knocking out the transient receptor potential vanilloid 4 (TRPV4), a member of the thermosensitive TRP channel family. ![]() We continuously measured the cross-sectional area of the brain slice for 150 min under macroscopic microscopy, finding that OGD induces swelling of brain slices. Here, we developed an in vitro model of ischemic stroke-induced edema in which male mouse brain slices were treated with oxygen-glucose deprivation (OGD) to mimic ischemia. Although brain edema is associated with a high fatality rate, the cellular and molecular processes of edema remain largely unclear. Brain edema is characterized by an increase in net brain water content, which results in an increase in brain volume.
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