Changes in hippocampal ultrastructure and gene expression of various nerve factors are strongly associated with the pathogenesis of epilepsy during seizure. Recent studies have shown that
(1) Mitochondrial dysfunction can lead to epileptic seizure, which can in turn further damage mitochondria.
(2) Bcl-2 can regulate apoptosis, and is strongly associated with changes in mitochondrial structure and function.
(3) Postsynaptic density-95 (PSD95) and synaptophysin play important roles in occurrence and development of traumatic epilepsy. However, little has been reported on how PSD95 and synaptophysin express at the onset of traumatic epilepsy, and whether PSD95 and synaptophysin participate in synapse reconstruction of forebrain circuit loop neurons following seizures.
In this tissue of NRR, four studies explored the changes in nerve factors in the hippocampus following epilepsy, using cell culture, molecular biological and morphological techniques and by examining P glycoprotein, gamma-aminobutyric acid B receptor, Bcl-2, PSD95 and synaptophysin expression in neurons of hippocampal subregions after epilepsy.

? Dynamic expression of P-glycoprotein in the CA1, CA3 and dentate gyrus of the rat hippocampus following lithium-pilocarpine-induced status epilepticus
Neural Regen Res. 2010;5(24):1851-1857.
       
? Effect of agonist on gamma-aminobutyric acid B receptor subunit expression in the hippocampus of epileptic rats
Neural Regen Res. 2009;4(8):577-582.

? Altered mitochondria and Bcl-2 expression in the hippocampal CA3 region in a rat model of acute epilepsy
Neural Regen Res. 2009;4(4):276-280.

? Correlation between synaptic protein expression and synaptic reorganization in the hippocampal CA3 region in a rat model of post-traumatic epilepsy
Neural Regen Res. 2010;5(15):1156-1160.