Alteration in Cngb1 expression upon maternal immune activation in a mouse model and its possible association with schizophrenia susceptibility
Hwayoung Lee 1, Sung Wook Kang 2, Hyeonjung Jeong 1, Jun-Tack Kwon 1, Young Ock Kim 1, Hak-Jae Kim 1*
1Department of Clinical Pharmacology, College of Medicine, Soonchunhyang University, Cheonan, 31151, Republic of Korea., 2Cardiovascular Center of Excellence, Louisiana State University Health Science Center, LA, 70112, USA
Received: July 31, 2020; Revised: October 20, 2020; Accepted: November 11, 2020; Published online: November 11, 2020.
© The Korean College of Neuropsychopharmacology. All rights reserved.

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 pathophysiology 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 schizophrenia 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 frequency 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.
Keywords: Cyclic nucleotide-gated channel subunit beta 1, Single nucleotide polymorphism, Maternal immune activation, Animal model, schizophrenia