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      Magnetic Resonance Spectroscopy in Schizophrenia: Evidence for Glutamatergic Dysfunction and Impaired Energy Metabolism

      research-article
      Author(s): 1 , 2 , , 3
      Publication date (Electronic):
      Journal: Neurochemical Research
      Publisher: Springer US
      Keywords: Glutamate, Glutamine, Schizophrenia, Metabolism, Magnetic resonance

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          Abstract

          In the past couple of decades, major efforts were made to increase reliability of metabolic assessments by magnetic resonance methods. Magnetic resonance spectroscopy (MRS) has been valuable for providing in vivo evidence and investigating biomarkers in neuropsychiatric disorders, namely schizophrenia. Alterations of glutamate and glutamine levels in brains of schizophrenia patients relative to healthy subjects are generally interpreted as markers of glutamatergic dysfunction. However, only a small fraction of MRS-detectable glutamate is involved in neurotransmission. Here we review and discuss brain metabolic processes that involve glutamate and that are likely to be implicated in neuropsychiatric disorders.

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          Pharmacology and functions of metabotropic glutamate receptors.

          P Conn, J P Pin (1997)
          In the mid to late 1980s, studies were published that provided the first evidence for the existence of glutamate receptors that are not ligand-gated cation channels but are coupled to effector systems through GTP-binding proteins. Since those initial reports, tremendous progress has been made in characterizing these metabotropic glutamate receptors (mGluRs), including cloning and characterization of cDNA that encodes a family of eight mGluR subtypes, several of which have multiple splice variants. Also, tremendous progress has been made in developing new highly selective mGluR agonists and antagonists and toward determining the physiologic roles of the mGluRs in mammalian brain. These findings have exciting implications for drug development and suggest that the mGluRs provide a novel target for development of therepeutic agents that could have a significant impact on neuropharmacology.
          Article 0 comments Cited 309 times – based on 0 reviews     Review now
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            Circuit-based framework for understanding neurotransmitter and risk gene interactions in schizophrenia.

            John Lisman, Joseph T. Coyle, Robert W. Green … (2008)
            Many risk genes interact synergistically to produce schizophrenia and many neurotransmitter interactions have been implicated. We have developed a circuit-based framework for understanding gene and neurotransmitter interactions. NMDAR hypofunction has been implicated in schizophrenia because NMDAR antagonists reproduce symptoms of the disease. One action of antagonists is to reduce the excitation of fast-spiking interneurons, resulting in disinhibition of pyramidal cells. Overactive pyramidal cells, notably those in the hippocampus, can drive a hyperdopaminergic state that produces psychosis. Additional aspects of interneuron function can be understood in this framework, as follows. (i) In animal models, NMDAR antagonists reduce parvalbumin and GAD67, as found in schizophrenia. These changes produce further disinhibition and can be viewed as the aberrant response of a homeostatic system having a faulty activity sensor (the NMDAR). (ii) Disinhibition decreases the power of gamma oscillation and might thereby produce negative and cognitive symptoms. (iii) Nicotine enhances the output of interneurons, and might thereby contribute to its therapeutic effect in schizophrenia.
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              Stress-induced alterations in prefrontal cortical dendritic morphology predict selective impairments in perceptual attentional set-shifting.

              Conor Liston, Melinda M. Miller, Deena S Goldwater … (2006)
              Stressful life events have been implicated clinically in the pathogenesis of mental illness, but the neural substrates that may account for this observation remain poorly understood. Attentional impairments symptomatic of these psychiatric conditions are associated with structural and functional abnormalities in a network of prefrontal cortical structures. Here, we examine whether chronic stress-induced dendritic alterations in the medial prefrontal cortex (mPFC) and orbital frontal cortex (OFC) underlie impairments in the behaviors that they subserve. After 21 d of repeated restraint stress, rats were tested on a perceptual attentional set-shifting task, which yields dissociable measures of reversal learning and attentional set-shifting, functions that are mediated by the OFC and mPFC, respectively. Intracellular iontophoretic injections of Lucifer yellow were performed in a subset of these rats to examine dendritic morphology in layer II/III pyramidal cells of the mPFC and lateral OFC. Chronic stress induced a selective impairment in attentional set-shifting and a corresponding retraction (20%) of apical dendritic arbors in the mPFC. In stressed rats, but not in controls, decreased dendritic arborization in the mPFC predicted impaired attentional set-shifting performance. In contrast, stress was not found to adversely affect reversal learning or dendritic morphology in the lateral OFC. Instead, apical dendritic arborization in the OFC was increased by 43%. This study provides the first direct evidence that dendritic remodeling in the prefrontal cortex may underlie the functional deficits in attentional control that are symptomatic of stress-related mental illnesses.
              Article 0 comments Cited 226 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                João M. N. Duarte: 0046 462 220 708 , joao.duarte@med.lu.se
                Journal
                Journal ID (nlm-ta): Neurochem Res
                Journal ID (iso-abbrev): Neurochem. Res
                Title: Neurochemical Research
                Publisher: Springer US (New York )
                ISSN (Print): 0364-3190
                ISSN (Electronic): 1573-6903
                Publication date (Electronic): 3 April 2018
                Publication date PMC-release: 3 April 2018
                Publication date (Print): 2019
                Volume: 44
                Issue: 1
                Pages: 102-116
                Affiliations
                [1 ]ISNI 0000 0001 0930 2361, GRID grid.4514.4, Department of Experimental Medical Science, Faculty of Medicine, , Lund University, ; BMC C11, Sölvegatan 19, 221 84 Lund, Sweden
                [2 ]ISNI 0000 0001 0930 2361, GRID grid.4514.4, Wallenberg Center for Molecular Medicine, , Lund University, ; Lund, Sweden
                [3 ]ISNI 0000000121839049, GRID grid.5333.6, Animal Imaging and Technology Core (AIT), Center for Biomedical Imaging (CIBM), , Ecole Polytechnique Fédérale de Lausanne, ; Lausanne, Switzerland
                Article
                Publisher ID: 2521
                DOI: 10.1007/s11064-018-2521-z
                PMC ID: 6345729
                PubMed ID: 29616444
                SO-VID: 2b08c75b-3f05-4bb5-b461-c447cad42df2
                Copyright © © The Author(s) 2018
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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.

                History
                Date received : 24 November 2017
                Date revision received : 28 March 2018
                Date accepted : 30 March 2018
                Categories
                Subject: Original Paper
                Custom metadata
                issue-copyright-statement © Springer Science+Business Media, LLC, part of Springer Nature 2019

                ScienceOpen disciplines: Neurosciences
                Keywords: glutamate,glutamine,schizophrenia,metabolism,magnetic resonance
                Data availability:
                ScienceOpen disciplines: Neurosciences
                Keywords: glutamate, glutamine, schizophrenia, metabolism, magnetic resonance

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