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      E-I Balance and Human Diseases – from Molecules to Networking

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          Abstract

          Information transfer in the brain requires a homeostatic control of neuronal excitability. Therefore, a functional balance between excitatory and inhibitory systems is established during development. This review contains recent information about the molecular mechanisms orchestrating the establishment and maintenance of this excitation-inhibition (E-I) balance, and it reviews examples of deregulation of inhibitory and excitatory systems at a molecular, network and disease level of investigation.

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          Most cited references60

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          Synaptic modifications in cultured hippocampal neurons: dependence on spike timing, synaptic strength, and postsynaptic cell type.

          Q Bi, G Bi, M Poo (1998)
          In cultures of dissociated rat hippocampal neurons, persistent potentiation and depression of glutamatergic synapses were induced by correlated spiking of presynaptic and postsynaptic neurons. The relative timing between the presynaptic and postsynaptic spiking determined the direction and the extent of synaptic changes. Repetitive postsynaptic spiking within a time window of 20 msec after presynaptic activation resulted in long-term potentiation (LTP), whereas postsynaptic spiking within a window of 20 msec before the repetitive presynaptic activation led to long-term depression (LTD). Significant LTP occurred only at synapses with relatively low initial strength, whereas the extent of LTD did not show obvious dependence on the initial synaptic strength. Both LTP and LTD depended on the activation of NMDA receptors and were absent in cases in which the postsynaptic neurons were GABAergic in nature. Blockade of L-type calcium channels with nimodipine abolished the induction of LTD and reduced the extent of LTP. These results underscore the importance of precise spike timing, synaptic strength, and postsynaptic cell type in the activity-induced modification of central synapses and suggest that Hebb's rule may need to incorporate a quantitative consideration of spike timing that reflects the narrow and asymmetric window for the induction of synaptic modification.
          Article 0 comments Cited 543 times – based on 0 reviews     Review now
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            Mutations of the X-linked genes encoding neuroligins NLGN3 and NLGN4 are associated with autism.

            Stéphane Jamain, Hélène Quach, Catalina Betancur … (2003)
            Many studies have supported a genetic etiology for autism. Here we report mutations in two X-linked genes encoding neuroligins NLGN3 and NLGN4 in siblings with autism-spectrum disorders. These mutations affect cell-adhesion molecules localized at the synapse and suggest that a defect of synaptogenesis may predispose to autism.
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              AMPA receptor trafficking and synaptic plasticity.

              Roberto Malinow, Robert Malenka (2002)
              Activity-dependent changes in synaptic function are believed to underlie the formation of memories. Two prominent examples are long-term potentiation (LTP) and long-term depression (LTD), whose mechanisms have been the subject of considerable scrutiny over the past few decades. Here we review the growing literature that supports a critical role for AMPA receptor trafficking in LTP and LTD, focusing on the roles proposed for specific AMPA receptor subunits and their interacting proteins. While much work remains to understand the molecular basis for synaptic plasticity, recent results on AMPA receptor trafficking provide a clear conceptual framework for future studies.
              Article 0 comments Cited 429 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Front Mol Neurosci
                Journal ID (publisher-id): Front. Mol. Neurosci.
                Title: Frontiers in Molecular Neuroscience
                Publisher: Frontiers Research Foundation
                ISSN (Electronic): 1662-5099
                Publication date (Electronic preprint): 29 January 2008
                Publication date (Electronic): 28 March 2008
                Publication date Collection: 2008
                Volume: 1
                Electronic Location Identifier: 2
                Affiliations
                [1] 1RNA Editing and Hyperexcitability Disorders Helmholtz Group, Max Delbrück Center for Molecular Medicine Berlin, Germany
                Author notes

                Edited by: Robert J. Harvey, University of London, UK

                Reviewed by: Alaa El-Husseini, University of British Columbia, Canada

                *Correspondence: Jochen C. Meier, Neuroscience Department, Max Delbrück Center for Molecular Medicine, Robert-Rössle-Strasse 10, 13092 Berlin, Germany. e-mail: jochen.meier@ 123456mdc-berlin.de
                Article
                DOI: 10.3389/neuro.02.002.2008
                PMC ID: 2526001
                PubMed ID: 18946535
                SO-VID: daa069f3-8eae-4c91-898c-d989f1cfcd06
                Copyright © Copyright © 2008 Eichler and Meier.
                License:

                This is an open-access article subject to an exclusive license agreement between the authors and the Frontiers Research Foundation, which permits unrestricted use, distribution, and reproduction in any medium, provided the original authors and source are credited.

                History
                Date received : 22 January 2008
                Date accepted : 30 January 2008
                Page count
                Figures: 1, Tables: 0, Equations: 0, References: 71, Pages: 5, Words: 5483
                Categories
                Subject: Neuroscience
                Subject: Perspective

                ScienceOpen disciplines: Neurosciences
                Keywords: schizophrenia,alzheimer's disease,epilepsy,autism,e-i balance,mental retardation,excitation,inhibition
                Data availability:
                ScienceOpen disciplines: Neurosciences
                Keywords: schizophrenia, alzheimer's disease, epilepsy, autism, e-i balance, mental retardation, excitation, inhibition

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