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Febrile seizures (FS) are the most common seizure disorders in children aged 6 months to 5 years. Children suffering from complex FS have a high risk of developing subsequent temporal lobe epilepsy (TLE). Canonical transient receptor potential channel (TRPC) members are identified as febrile seizure (FS)-related genes in hyperthermia prone rats. However, the role of TRPC3 in hyperthermia-induced FS rats remains unclear. The purpose of this study focused on exploring whether TRPC3 regulated NCX3 expression further affected seizuresd evelopment. In thepresent study, we demonstrated that TRPC3expression was significantly increased at both the protein and mRNA levels after hyperthermia induced FS rats and rat hippocampalneuron cells.The specific inhibitor of TRPC3, remarkably attenuated the susceptibility and severity of seizures, neuronal cell death,and neuroinflammation in FS rats. In contrast, NCX3 activation was significantly suppressed in recurent FS rats and rat hippocampal neuron cells. The expression of NCX3 wasupregulated after TRPC3 inhibition in vivo and in vitro. Furthermore, The TRPC3 inhibitors suppressed Ca2+ transients in response to hyperthermia-induces febrile seizure. Taken together, our findings demonstrate thatTRPC3 functions as a critical regulator of seizure susceptibility and the TRPC3 inhibitormay be a viable option for FS therapeutics.

Febrile Seizure;Canonical transient receptor potential channel 3