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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 Ca(2+) 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 (Cng...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Korean College of Neuropsychopharmacology
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8553526/ https://www.ncbi.nlm.nih.gov/pubmed/34690117 http://dx.doi.org/10.9758/cpn.2021.19.4.618 |
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author | Lee, Hwayoung Kang, Sung Wook Jeong, Hyeonjung Kwon, Jun-Tack Kim, Young Ock Kim, Hak-Jae |
author_facet | Lee, Hwayoung Kang, Sung Wook Jeong, Hyeonjung Kwon, Jun-Tack Kim, Young Ock Kim, Hak-Jae |
author_sort | Lee, Hwayoung |
collection | PubMed |
description | OBJECTIVE: The cyclic nucleotide-gated channel (Cng) regulates synaptic efficacy in brain neurons by modulating Ca(2+) 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. |
format | Online Article Text |
id | pubmed-8553526 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Korean College of Neuropsychopharmacology |
record_format | MEDLINE/PubMed |
spelling | pubmed-85535262021-11-30 Alteration in Cngb1 Expression upon Maternal Immune Activation in a Mouse Model and Its Possible Association with Schizophrenia Susceptibility Lee, Hwayoung Kang, Sung Wook Jeong, Hyeonjung Kwon, Jun-Tack Kim, Young Ock Kim, Hak-Jae Clin Psychopharmacol Neurosci Original Article OBJECTIVE: The cyclic nucleotide-gated channel (Cng) regulates synaptic efficacy in brain neurons by modulating Ca(2+) 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. Korean College of Neuropsychopharmacology 2021-11-30 2021-11-30 /pmc/articles/PMC8553526/ /pubmed/34690117 http://dx.doi.org/10.9758/cpn.2021.19.4.618 Text en Copyright© 2021, Korean College of Neuropsychopharmacology https://creativecommons.org/licenses/by-nc/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0 (https://creativecommons.org/licenses/by-nc/4.0/) ) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Lee, Hwayoung Kang, Sung Wook Jeong, Hyeonjung Kwon, Jun-Tack Kim, Young Ock Kim, Hak-Jae Alteration in Cngb1 Expression upon Maternal Immune Activation in a Mouse Model and Its Possible Association with Schizophrenia Susceptibility |
title | Alteration in Cngb1 Expression upon Maternal Immune Activation in a Mouse Model and Its Possible Association with Schizophrenia Susceptibility |
title_full | Alteration in Cngb1 Expression upon Maternal Immune Activation in a Mouse Model and Its Possible Association with Schizophrenia Susceptibility |
title_fullStr | Alteration in Cngb1 Expression upon Maternal Immune Activation in a Mouse Model and Its Possible Association with Schizophrenia Susceptibility |
title_full_unstemmed | Alteration in Cngb1 Expression upon Maternal Immune Activation in a Mouse Model and Its Possible Association with Schizophrenia Susceptibility |
title_short | Alteration in Cngb1 Expression upon Maternal Immune Activation in a Mouse Model and Its Possible Association with Schizophrenia Susceptibility |
title_sort | alteration in cngb1 expression upon maternal immune activation in a mouse model and its possible association with schizophrenia susceptibility |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8553526/ https://www.ncbi.nlm.nih.gov/pubmed/34690117 http://dx.doi.org/10.9758/cpn.2021.19.4.618 |
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