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      Structural bases for central nervous system malfunction in thequakingmouse: Dysmyelination in a potential model of schizophrenia

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      Journal: Journal of Neuroscience Research
      Publisher: Wiley-Blackwell

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          Abnormal neural oscillations and synchrony in schizophrenia.

          Peter Uhlhaas, Wolf Singer (2010)
          Converging evidence from electrophysiological, physiological and anatomical studies suggests that abnormalities in the synchronized oscillatory activity of neurons may have a central role in the pathophysiology of schizophrenia. Neural oscillations are a fundamental mechanism for the establishment of precise temporal relationships between neuronal responses that are in turn relevant for memory, perception and consciousness. In patients with schizophrenia, the synchronization of beta- and gamma-band activity is abnormal, suggesting a crucial role for dysfunctional oscillations in the generation of the cognitive deficits and other symptoms of the disorder. Dysfunctional oscillations may arise owing to anomalies in the brain's rhythm-generating networks of GABA (gamma-aminobutyric acid) interneurons and in cortico-cortical connections.
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            White matter in learning, cognition and psychiatric disorders.

            R. Douglas Fields (2008)
            White matter is the brain region underlying the gray matter cortex, composed of neuronal fibers coated with electrical insulation called myelin. Previously of interest in demyelinating diseases such as multiple sclerosis, myelin is attracting new interest as an unexpected contributor to a wide range of psychiatric disorders, including depression and schizophrenia. This is stimulating research into myelin involvement in normal cognitive function, learning and IQ. Myelination continues for decades in the human brain; it is modifiable by experience, and it affects information processing by regulating the velocity and synchrony of impulse conduction between distant cortical regions. Cell-culture studies have identified molecular mechanisms regulating myelination by electrical activity, and myelin also limits the critical period for learning through inhibitory proteins that suppress axon sprouting and synaptogenesis.
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              Axon-glia interactions and the domain organization of myelinated axons requires neurexin IV/Caspr/Paranodin.

              Manzoor A. Bhat, Jose C. Rios, Yue H Lu … (2001)
              Myelinated fibers are organized into distinct domains that are necessary for saltatory conduction. These domains include the nodes of Ranvier and the flanking paranodal regions where glial cells closely appose and form specialized septate-like junctions with axons. These junctions contain a Drosophila Neurexin IV-related protein, Caspr/Paranodin (NCP1). Mice that lack NCP1 exhibit tremor, ataxia, and significant motor paresis. In the absence of NCP1, normal paranodal junctions fail to form, and the organization of the paranodal loops is disrupted. Contactin is undetectable in the paranodes, and K(+) channels are displaced from the juxtaparanodal into the paranodal domains. Loss of NCP1 also results in a severe decrease in peripheral nerve conduction velocity. These results show a critical role for NCP1 in the delineation of specific axonal domains and the axon-glia interactions required for normal saltatory conduction.
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                Author and article information

                Journal
                Title: Journal of Neuroscience Research
                Abbreviated Title: J. Neurosci. Res.
                Publisher: Wiley-Blackwell
                ISSN: 03604012
                Publication date Created: March 2013
                Publication date (Print): March 2013
                Volume: 91
                Issue: 3
                Pages: 374-381
                Article
                DOI: 10.1002/jnr.23167
                SO-VID: 9f05c9d1-5b31-4777-96b8-0433b1ad7c10
                Copyright © © 2013
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                http://doi.wiley.com/10.1002/tdm_license_1.1

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