**5. Conclusions**

The present data provide novel evidence that TRPC6 regulates LONP1 expression via ERK1/2 activity. In brief, TRPC6-mediated ERK1/2 activation increased LONP1 expression and facilitated mitochondrial fission. Thus, TRPC6 may be involved in the quality controls of mitochondria as well as mitochondrial dynamics, which would enhance DGC invulnerability to SE (Figure 6). To the best of our knowledge, the present study is the first indication of the role of the TRPC6-ERK1/2-LONP1 pathway in neuronal vulnerability to SE. Therefore, this signaling pathway will be an interesting and important therapeutic target for neuroprotection from various neurological diseases.

**Supplementary Materials:** The following are available online at http://www.mdpi.com/2073-4409/8/11/1376/s1, Figure S1: Representative photos of mitochondria for each siRNA or compound treated-animals. Figure S2: Full-length gel images of Western blot data in Figure 1D. Figure S3: Full-length gel images of Western blot data in Figure 2A. Figure S4: Full-length gel images of Western blot data in Figure 3A.

**Author Contributions:** T.-C.K. designed and supervised the project. J.-E.K., H.P., S.-H.C. and M.-J.K. performed the experiments described in the manuscript. J.-E.K. and T.-C.K. analyzed the data, and wrote the manuscript.

**Funding:** This study was supported by a gran<sup>t</sup> of National Research Foundation of Korea (NRF) gran<sup>t</sup> (No. 2018R1C1B6005216 and No. 2018R1A2A2A05018222). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

**Conflicts of Interest:** The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
