Literature DB >> 19435655

Loss of function of glial gap junctions may cause severe cognitive impairments in schizophrenia.

Bernhard Mitterauer1.   

Abstract

A generalized cognitive deficit is at the core of schizophrenia. It is hypothesized that a loss of function of glial gap junctions may cause severe cognitive impairment in schizophrenia. Glial gap junctions are electrical channels that may register the neuronal activation frequencies of glial-neuronal compartments by generating gap junction plaques. The various proteins (connexins) of gap junctions may be capable to differentiate between the operation qualities of the cognate synapses defined by the neurotransmitter types. Thus, the brain is capable of distinguishing between different cognitive qualities (domains or categories). If the function of glial gap junction proteins is lost, the brain is incapable to distinguish between same and different qualities of information processing. Dependent on the brain regions affected, this disorder may be responsible for severe cognitive impairment in schizophrenia. Finally, general approaches for testing the hypothesis are outlined.

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Year:  2009        PMID: 19435655     DOI: 10.1016/j.mehy.2009.04.003

Source DB:  PubMed          Journal:  Med Hypotheses        ISSN: 0306-9877            Impact factor:   1.538


  7 in total

1.  Association study between polymorphisms of the PARD3 gene and schizophrenia.

Authors:  Su Kang Kim; Jong Yoon Lee; Hae Jeong Park; Jong Woo Kim; Joo-Ho Chung
Journal:  Exp Ther Med       Date:  2012-02-23       Impact factor: 2.447

2.  Possible effects of synaptic imbalances on oligodendrocyte-axonic interactions in schizophrenia: a hypothetical model.

Authors:  Bernhard J Mitterauer; Birgitta Kofler-Westergren
Journal:  Front Psychiatry       Date:  2011-04-12       Impact factor: 4.157

3.  Clozapine Normalizes a Glutamatergic Transmission Abnormality Induced by an Impaired NMDA Receptor in the Thalamocortical Pathway via the Activation of a Group III Metabotropic Glutamate Receptor.

Authors:  Kouji Fukuyama; Ryo Kato; Masahiko Murata; Takashi Shiroyama; Motohiro Okada
Journal:  Biomolecules       Date:  2019-06-17

4.  Activation of Astroglial Connexin is Involved in Concentration-Dependent Double-Edged Sword Clinical Action of Clozapine.

Authors:  Kouji Fukuyama; Ruri Okubo; Masahiko Murata; Takashi Shiroyama; Motohiro Okada
Journal:  Cells       Date:  2020-02-11       Impact factor: 6.600

5.  Effects of Atypical Antipsychotics, Clozapine, Quetiapine and Brexpiprazole on Astroglial Transmission Associated with Connexin43.

Authors:  Kouji Fukuyama; Motohiro Okada
Journal:  Int J Mol Sci       Date:  2021-05-25       Impact factor: 5.923

6.  Identification of de novo mutations in prenatal neurodevelopment-associated genes in schizophrenia in two Han Chinese patient-sibling family-based cohorts.

Authors:  Shan Jiang; Daizhan Zhou; Yin-Ying Wang; Peilin Jia; Chunling Wan; Xingwang Li; Guang He; Dongmei Cao; Xiaoqian Jiang; Kenneth S Kendler; Ming Tsuang; Travis Mize; Jain-Shing Wu; Yimei Lu; Lin He; Jingchun Chen; Zhongming Zhao; Xiangning Chen
Journal:  Transl Psychiatry       Date:  2020-09-01       Impact factor: 6.222

Review 7.  A Working Hypothesis Regarding Identical Pathomechanisms between Clinical Efficacy and Adverse Reaction of Clozapine via the Activation of Connexin43.

Authors:  Motohiro Okada; Kouji Fukuyama; Takashi Shiroyama; Masahiko Murata
Journal:  Int J Mol Sci       Date:  2020-09-24       Impact factor: 5.923

  7 in total

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