Alteration in Cngb1 Expression upon Maternal Immune Activation in a Mouse Model and Its Possible Association with Schizophrenia Susceptibility

Objective: The cyclic nucleotide-gated channel (Cng) regulates synaptic efficacy in brain neurons by modulating Ca2+ levels in response to changes in cyclic nucleotide concentrations. This study investigated whether the expression of Cng channel, cyclic nucleotide-gated channel subunit beta 1 (Cngb1) exhibited any relationship with the pathophysiol-ogy of schizophrenia in an animal model and whether genetic polymorphisms of the human gene were associated with the progression of schizophrenia in a Korean population. Methods: We investigated whether Cngb1 expression was related to psychiatric disorders in a mouse model of schizo-phrenia induced by maternal immune activation. A case-control study was conducted of 275 schizophrenia patients and 410 controls with single-nucleotide polymorphisms (SNPs) in the 5 '-near region of CNGB1. Results: Cngb1 expression was decreased in the prefrontal cortex in the mouse model. Furthermore, the genotype fre-quency of a SNP (rs3756314) of CNGB1 was associated with the risk of schizophrenia. Conclusion: Our results suggest that CNGB1 might be associated with schizophrenia susceptibility and maternal immune activation. Consequently, it is hypothesized that CNGB1 may be involved in the pathophysiology of schizophrenia.

Automated summary

The study found that the expression of Cngb1 decreased in a mouse model of schizophrenia, and a SNP in the human CNGB1 gene was associated with the risk of schizophrenia. This suggests that CNGB1 may be involved in the pathophysiology of schizophrenia.