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Levels of the growth-associated protein GAP-43 are selectively increased in association cortices in schizophrenia

Perrone-Bizzozero, Nora I., Sower, Angela C., Bird, Edward D., Benowitz, Larry I., Ivins, Kathryn J., Neve, Rachael L.·1996·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.93.24.14182
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Abstract

The pathophysiology of schizophrenia may involve perturbations of synaptic organization during development. The presence of cytoarchitectural abnormalities that may reflect such perturbations in the brains of patients with this disorder has been well-documented. Yet the mechanistic basis for these features of the disorder is still unknown. We hypothesized that altered regulation of the neuronal growth-associated protein GAP-43, a membrane phosphoprotein found at high levels in the developing brain, may play a role in the alterations in brain structure and function observed in schizophrenia. In the mature human brain, GAP-43 remains enriched primarily in association cortices and in the hippocampus, and it has been suggested that this protein marks circuits involved in the acquisition, processing, and/or storage of new information. Because these processes are known to be altered in schizophrenia, we proposed that GAP-43 levels might be altered in this disorder. Quantitative immunoblots revealed that the expression of GAP-43 is increased preferentially in the visual association and frontal cortices of schizophrenic patients, and that these changes are not present in other neuropsychiatric conditions requiring similar treatments. Examination of the levels of additional markers in the brain revealed that the levels of the synaptic vesicle protein synaptophysin are reduced in the same areas, but that the abundance of the astrocytic marker of neurodegeneration, the glial fibrillary acidic protein, is unchanged. In situ hybridization histochemistry was used to show that the laminar pattern of GAP-43 expression appears unaltered in schizophrenia. We propose that schizophrenia is associated with a perturbed organization of synaptic connections in distinct cortical associative areas of the human brain, and that increased levels of GAP-43 are one manifestation of this dysfunctional organization.

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  • These changes may be caused by the neurotrophic effects of reduced NMDA-R inputs and a loss of synaptic connectivity.

    “These changes may be caused by the neurotrophic effects of reduced NMDA-R inputs (Rajan and Cline, 1998; Monfils and Teskey, 2004) and a loss of synaptic connectivity (Perrone-Bizzozero et al., 1996; Glantz and Lewis, 1997)”

    From The Computational Anatomy of Psychosis (2013) · cites this paper as Perrone-Bizzozero et al., 1996

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Authors
Perrone-Bizzozero, N. I., Sower, A. C., Bird, E. D., Benowitz, L. I., Ivins, K. J., & Neve, R. L.
Affiliations
Departments of Biochemistry and Chemistry, University of New Mexico School of Medicine, Albuquerque, NM 87131; Departments of Neuropathology and Genetics, McLean Hospital, Harvard Medical School, Belmont, MA 02178; and Department of Neurosurgery, The Children’s Hospital, Harvard Medical School, Boston, MA 02115
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
1996-11-26
Volume
93
Issue
24
Pages
14182-14187
ISSN
  • 0027-8424
  • 1091-6490
DOI
10.1073/pnas.93.24.14182
Cited by
162
References
0
Language
en

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