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      Electrophysiological evidence for abnormal glutamate-GABA association following psychosis onset

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          Abstract

          Previous studies have shown glutamatergic dysfunction and γ-aminobutyric acid (GABA)-ergic dysfunction in schizophrenia. Animal studies suggest that N-methyl- d-aspartate receptor (NMDAR) dysfunction and GABA-ergic dysfunction interact with each other and lead to alterations in excitatory/inhibitory balance. The NMDAR and GABAergic-interneuron functions may be indexed by mismatch negativity (MMN) and auditory steady-state gamma-band response (ASSR), respectively. However, no previous studies have tested the hypothesis of an abnormal association between MMN and gamma-band ASSR in the same patients to identify the in vivo evidence of NMDAR-GABA association during the early stages of psychosis. Participants were individuals with recent-onset schizophrenia (ROSZ; N = 21), ultra-high risk (UHR; N = 27), and healthy controls (HCs; N = 24). The MMN amplitude was significantly impaired in ROSZ ( p = 0.001, d= 1.20) and UHR ( p = 0.003, d= 1.01) compared with HCs. The intertrial phase coherence (ITC) index of gamma-band ASSR was significantly reduced in ROSZ compared with HCs ( p < 0.001, d=1.27) and UHR ( p = 0.032, d=0.75). The event-related spectral perturbation (ERSP) index of gamma-band ASSR was significantly smaller in ROSZ compared with HCs ( p < 0.001, d = −1.21). The MMN amplitude was significantly correlated with the ITC in ROSZ ( r = −0.69, p < 0.001). These findings provide the first in vivo evidence that an abnormal association of the electrophysiological indices of NMDAR and GABA dysfunctions may be present in recent-onset schizophrenia.

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          Most cited references 67

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          The positive and negative syndrome scale (PANSS) for schizophrenia.

          The variable results of positive-negative research with schizophrenics underscore the importance of well-characterized, standardized measurement techniques. We report on the development and initial standardization of the Positive and Negative Syndrome Scale (PANSS) for typological and dimensional assessment. Based on two established psychiatric rating systems, the 30-item PANSS was conceived as an operationalized, drug-sensitive instrument that provides balanced representation of positive and negative symptoms and gauges their relationship to one another and to global psychopathology. It thus constitutes four scales measuring positive and negative syndromes, their differential, and general severity of illness. Study of 101 schizophrenics found the four scales to be normally distributed and supported their reliability and stability. Positive and negative scores were inversely correlated once their common association with general psychopathology was extracted, suggesting that they represent mutually exclusive constructs. Review of five studies involving the PANSS provided evidence of its criterion-related validity with antecedent, genealogical, and concurrent measures, its predictive validity, its drug sensitivity, and its utility for both typological and dimensional assessment.
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            Global assessment of functioning. A modified scale.

             Richard Hall (1995)
            The modified Global Assessment of Functioning (GAF) scale has more detailed criteria and a more structured scoring system than the original GAF. The two scales were compared for reliability and validity. Raters who had different training levels assigned hospital admission and discharge GAF scores from patient charts. Intraclass correlation coefficients for admission GAF scores were higher for raters who used the modified GAF (0.81), compared with raters who used the original GAF (0.62). Validity studies showed a high correlation (0.80) between the two sets of scores. The modified GAF also correlated well with Zung Depression scores (-0.73). The modified GAF may be particularly useful when interrater reliability needs to be maximum and/or when persons with varying skills and employment backgrounds--and without much GAF training--must rate patients. Because of the increased structure, the modified GAF may also be more resistant to rater bias.
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              Postnatal NMDA receptor ablation in corticolimbic interneurons confers schizophrenia-like phenotypes.

              Cortical GABAergic dysfunction may underlie the pathophysiology of psychiatric disorders, including schizophrenia. Here, we characterized a mouse strain in which the essential NR1 subunit of the NMDA receptor (NMDAR) was selectively eliminated in 40-50% of cortical and hippocampal interneurons in early postnatal development. Consistent with the NMDAR hypofunction theory of schizophrenia, distinct schizophrenia-related symptoms emerged after adolescence, including novelty-induced hyperlocomotion, mating and nest-building deficits, as well as anhedonia-like and anxiety-like behaviors. Many of these behaviors were exacerbated by social isolation stress. Social memory, spatial working memory and prepulse inhibition were also impaired. Reduced expression of glutamic acid decarboxylase 67 and parvalbumin was accompanied by disinhibition of cortical excitatory neurons and reduced neuronal synchrony. Postadolescent deletion of NR1 did not result in such abnormalities. These findings suggest that early postnatal inhibition of NMDAR activity in corticolimbic GABAergic interneurons contributes to the pathophysiology of schizophrenia-related disorders.
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                Author and article information

                Contributors
                +81-3-5800-8919 , kasaik-tky@umin.net
                Journal
                Transl Psychiatry
                Transl Psychiatry
                Translational Psychiatry
                Nature Publishing Group UK (London )
                2158-3188
                8 October 2018
                8 October 2018
                2018
                : 8
                Affiliations
                [1 ]ISNI 0000 0001 2151 536X, GRID grid.26999.3d, Department of Neuropsychiatry, Graduate School of Medicine, , The University of Tokyo, ; 7-3-1, Hongo, Bunkyo-ku, Tokyo 113-8655 Japan
                [2 ]ISNI 0000 0001 2151 536X, GRID grid.26999.3d, The International Research Center for Neurointelligence (WPI-IRCN) at The University of Tokyo Institutes for Advanced Study (UTIAS), The University of Tokyo, ; 7-3-1, Hongo, Bunkyo-ku, Tokyo 113-8655 Japan
                [3 ]Department of Psychiatry, Kawamuro Memorial Hospital, 71, Kitashinbo, Joetsu-shi, Niigata 943-0109 Japan
                [4 ]ISNI 0000 0001 2151 536X, GRID grid.26999.3d, University of Tokyo Institute for Diversity & Adaptation of Human Mind (UTIDAHM), 3-8-1, Komaba, ; Meguro-ku, Tokyo 153-8902 Japan
                [5 ]ISNI 0000 0001 2151 536X, GRID grid.26999.3d, Center for Evolutionary Cognitive Sciences, Graduate School of Art and Sciences, The University of Tokyo, 3-8-1, Komaba, ; Meguro-ku, Tokyo 153-8902 Japan
                [6 ]ISNI 0000 0001 2151 536X, GRID grid.26999.3d, Department of Rehabilitation, Graduate School of Medicine, , The University of Tokyo, 7-3-1, Hongo, ; Bunkyo-ku, Tokyo 113-8655 Japan
                Article
                261
                10.1038/s41398-018-0261-0
                6175929
                © The Author(s) 2018

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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                Clinical Psychology & Psychiatry

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