TRPC6-Mediated ERK1/2 Activation Increases Dentate Granule Cell Resistance to Status Epilepticus Via Regulating Lon Protease-1 Expression and Mitochondrial Dynamics.
In the present study, status epilepticus (SE, a prolonged seizure activity) led to reactive astrogliosis showing the increases in GFAP expression and the number of proliferating astrocytes with prolonged extracellular signal receptor-activated kinases 1/2 (ERK1/2) activation and reduced nuclear p27<sup>Kip1</sup> level.
These findings indicate that TRPC6 may regulate mitochondrial dynamics via ERK1/2-mediaed DRP1 activation, which would be involved in DGC invulnerability to SE.