Schizophrenia is a severe psychiatric disorder with unknown etiology. Currently, a combination of genetic and environmental factors underlying the development of this disorder is discussed. Genetic association and genome-wide association studies revealed several risk genes of schizophrenia, among them are neuregulin1, DISC1, D-amino-acid oxidase activator (DAOA/G72), zinc finger protein 804A (ZNF804A), transcription factor 4 (TCF4) [32]. Environmental factors such as obstetric complications with hypoxia [37], prenatal infection, season of birth, drug abuse, and migration [29] may interact with genetic factors, influencing onset and progression of the disease. This gene-environmental interaction may comprise epigenetic alterations like DNA methylation and histone acetylation [35, 41]. An interaction between metabotropic glutamate receptor (GRM3) gene variants and severe obstetric complications on hippocampus volume has been reported, but this finding was not specific for schizophrenia [22]. Furthermore, it is assumed that these risk factors may affect brain tissue during perinatal neurodevelopment and may lead to the onset of psychotic symptoms in early adulthood during the synaptic pruning process of the prefrontal cortex [43]. In early adulthood, animal models of neonatal hippocampal lesions show behavioral deficits comparable
