Hippocampal Pathophysiology: Commonality Shared by Temporal Lobe Epilepsy and Psychiatric Disorders

Figure 3

A schematic representation of the shared pathophysiology from genetic level to behavior level across α-CaMKII hKO mice, psychiatric patients, and patients with TLE. A mutation of CAMK2A gene was found in patients with schizophrenia and it is also implicated in bipolar disorder [72, 73]. α-CaMKII hKO mice have behavioral deficits [63] which are observed in patients with schizophrenia and TLE [74, 75]. Furthermore, α-CaMKII hKO animals were shown to have immaturation of granular cells in DG which was also observed in patients [74]. Importantly, the α-CaMKII hKO mouse showed the neuronal hyperactivity [63, 64] that matches to the observed hyperactivity in the hippocampus in patients [33, 38, 65, 66]. These shared features and the having history of febrile seizure in patients lead us to hypothesize the presence of mossy fiber misguidance [76] in patients with schizophrenia.