Clinical Psychopharmacology and Neuroscience Papers in Press available online.

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
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.
Accepted Manuscript [Submitted on 2020-07-31, Accepted on 2020-11-11]