COX-2/PGE2 axis regulates hippocampal BDNF/TrkB signaling via EP2 receptor after prolonged seizures.

The molecular mechanisms whereby BDNF/TrkB signaling is upregulated in the hippocampus by SE largely remain unknown. Our findings suggest that COX-2 via the PGE2/EP2 pathway regulates hippocampal BDNF/TrkB activity following prolonged seizures. EP2 inhibition by our bioavailable and brain-permeable antagonists such as TG6-10-1 might therefore provide a novel strategy to suppress the abnormal TrkB activity, an event that can sufficiently trigger pathogenic processes within the brain including acquired epileptogenesis.