Abstract
Schizophrenia is a complex psychiatric mental disorder often characterized by abnormal social behavior and failure to recognize what is real. Common symptoms include false beliefs, unclear or confused thinking, auditory hallucinations, reduced social engagement and emotional expression, and inactivity. Neuroontogenetic theory explains the occurrence of disease events taken place during intrauterine period. Gutamatergic signaling interferes with ethion-pathogenic mechanisms of schizophrenia. The disease is associated with N-methyl-D-aspartate NMDA receptor hypofunction and a number of genes suspected in respect of schizophrenia influence on a NMDA receptor signaling. NRG1 and ErbB4 its receptor involved in the glutamatergic signaling by regulating the NMDA receptor complex. Neuregulins are signaling proteins structurally related to the epidermal growth factor (EGF). The mechanisms underlying the contribution of NRG1/ErbB4 system to schizophrenia pathophysiology remain insignificant, but they reveal only after the complete maturation of the brain. Prenatal stress in rats simulates many of the cognitive and sensory deficits manifest in the disease. Identified in this experimental model deficits in immunochistochemical expression of Neuroregulin1- ErbB4- system directed changes at the molecular level in the hippocampus, a brain structure with a role in the regulation of stress.
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