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Research Article| Volume 27, ISSUE 9, P1038-1044, May 01, 1990

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Deficit and hemispheric asymmetry of GABA uptake sites in the hippocampus in schizophrenia

  • Gavin P. Reynolds
    Correspondence
    Address reprint requests to Gavin P. Reynolds, Department of Biomedical Science, The University of Sheffield, Sheffield UK S10 2TN.
    Affiliations
    Department of Pathology, University of Nottingham Medical School, Queen's Medical Centre, Nottingham, United Kingdom

    Institute of Psychiatry, De Crespigny Park, Denmark Hill, London, UK
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  • Carole Czudek
    Affiliations
    Department of Pathology, University of Nottingham Medical School, Queen's Medical Centre, Nottingham, United Kingdom

    Institute of Psychiatry, De Crespigny Park, Denmark Hill, London, UK
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  • Harry B. Andrews
    Affiliations
    Department of Pathology, University of Nottingham Medical School, Queen's Medical Centre, Nottingham, United Kingdom

    Institute of Psychiatry, De Crespigny Park, Denmark Hill, London, UK
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DOI:https://doi.org/10.1016/0006-3223(90)90039-5
Deficit and hemispheric asymmetry of GABA uptake sites in the hippocampus in schizophrenia
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      Abstract

      There is increasing evidence of a deficit or disturbance of neurons in the brains of schizophrenic patients—evidence that particularly implicates the frontal or temporal lobes. As yet there is no direct neurochemical correlate of the transmitter systems involved, although changes in some neurotransmitters in the temporal lobe have been reported. Radiolabeled nipecotic acid, a specific inhibitor of uptake sites to gamma-aminobutyric acid (GABA), has provided a marker of GABAergic neurons. The binding of this ligand to brain tissue taken at autopsy has demonstrated a decreased density of GABA uptake sites in the hippocampus in schizophrenia. This decrease was found to correlate in the left hemisphere with increased concentration of dopamine in the amygdala, providing a link between neuropathology, evidence of laterality, and the dopamine hypothesis of the disease.
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      Article info

      Publication history

      Received in revised form: August 4, 1989
      Received: June 8, 1989

      Identification

      DOI: https://doi.org/10.1016/0006-3223(90)90039-5

      Copyright

      © 1990 Published by Elsevier Inc.

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