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A hallmark of temporal lobe epilepsy (TLE) is hippocampal neuronal demise and aberrant mossy fiber sprouting. In addition, unrestrained neuronal activity in TLE patients induces gene expression including immediate early genes (IEGs) such as  Fos  and  Egr1 .  We employed the mouse pilocarpine model to analyze the transcription factor (TF) serum response factor (SRF) in epileptogenesis, seizure induced histopathology and IEG induction. SRF is a neuronal activity regulated TF stimulating IEG expression as well as nerve fiber growth and guidance. Adult conditional SRF deficient mice ( Srf    CaMKCreERT2  ) were more refractory to initial  status epilepticus  (SE) acquisition. Further, SRF deficient mice developed more spontaneous recurrent seizures (SRS). Genome-wide transcriptomic analysis uncovered a requirement of SRF for SE and SRS induced IEG induction (e.g.  Fos, Egr1, Arc ,  Npas4 ,  Btg2 ,  Atf3) . SRF was required for epilepsy associated neurodegeneration, mossy fiber sprouting and inflammation. We uncovered MAP kinase signaling as SRF target during epilepsy. Upon SRF ablation, seizure evoked induction of dual specific phosphatases ( Dusp5  and  Dusp6 ) was reduced. Lower expression of these negative ERK kinase regulators correlated with altered P-ERK levels in epileptic  Srf  mutant animals.  Overall, this study uncovered an SRF contribution to several processes of epileptogenesis in the pilocarpine model.   Electronic supplementary material  The online version of this article (doi:10.1186/s13041-017-0310-2) contains supplementary material, which is available to authorized users.

SRF modulates seizure occurrence, activity induced gene transcription and hippocampal circuit reorganization in the mouse pilocarpine epilepsy model