G Proteins in the Medial Temporal Lobe in Schizophrenia

  • Fumihiko Okada
Part of the Neuromethods book series (NM, volume 31)

Abstract

Numerous controlled investigations by computed tomography and magnetic resonance imaging of living patients suffering from schizophrenia have found quantitative evidence of brain pathology in the form of enlarged third and lateral ventricles and increased cortical markings suggestive of reduced gyral mass or atrophy (Johnstone et al., 1976; Shelton and Weinberger, 1986; Suddath et al., 1989). In addition, controlled studies of postmortem brain tissue have found nonspecific, but objective evidence of abnormal brain structure in the periventricular limbic and diencephalic areas in schizophrenia (Lesch and Bogerts, 1984; Bogerts et al., 1985; Brown et al., 1986; Jakob and Beckmann, 1986; Roberts, 1990). Crow et al. (1989) showed asymmetrical enlargement of the temporal horn of the lateral cerebral ventricle in schizophrenia. These structural abnormalities occur in the absence of degenerative changes in the brain. It has been proposed on the basis of these studies that some anomaly of growth occurs during brain development, but little neurochemical evidence has yet been found that correlates with these structural findings.

Keywords

Schizophrenic Patient Medial Temporal Lobe Lipid Modification Abnormal Brain Structure Lateral Cerebral Ventricle 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

References

  1. Asano, T., Semba R, Ogasawara N., and Kato K. (1987) Highly sensitive immunoassay for the a-subunit of the GTP-binding protein Go and its regional distribution in bovine brain. J. Neurochem. 48, 1617–1623.PubMedCrossRefGoogle Scholar
  2. Asano T., Morishita R, Semba R., Itoh, H., Kaziro, Y, and Kato K. (1989) Identification of lung major GTP-binding protein as Gi2 and its distribution in various rat tissues determined by immunoassay. Biochemistry 28, 4749–4754.PubMedCrossRefGoogle Scholar
  3. Asano, T., Shmohara, H., Morishita, R, and Kato, K. (1990) Immunochemlcal and lmmunohistochernical localization of the G protein Gil in rat central nervous tissues. J Biochem. 108, 988–994PubMedGoogle Scholar
  4. Bogerts, B., Meertz, E, and Schonfeld-Bausch, R. (1985) Basal ganglia and limbic system pathology in schizophrenia: a morphometric study of brain volume and shrinkage. Arch. Gen. Psychiatry 42, 784–791.PubMedGoogle Scholar
  5. Brown, R., Colter, N., Corsellis J. A N., Crow, T J., Frith, C. D., Jagoe, R., Johnstone, E. C, and Marsh, L (1986) Postmortem evidence of structural brain changes in schizophrenia Differences in brain weight, temporal horn area, and parahippocampal gyrus compared with affective disorder Arch. Gen. Psychiatry 43, 36–42.PubMedGoogle Scholar
  6. Crow, T. J., Ball, J., Bloom, S R., Brown, R., Bruton, C. J., Colter, N., Frith, C. D, Johnstone, E. C, Owens, D. G. C, and Roberts, G. W. (1989) Schizophrenia as an anomaly of development of cerebral asymmetry. A postmortem study and a proposal concernmg the genetic basis of the disease. Arch Gen. Psychiatry 46, 1145–1150.PubMedGoogle Scholar
  7. Feighner, J. P., Robins, E., Guze, S. B., Woodruff, R. A., Winokur, G., and Munoz, R. (1972) Diagnostic criteria for use in psychiatric research. Arch. Gen Psychiatry 26, 57–63PubMedGoogle Scholar
  8. Graziano, M. P. and Gilman, A G. (1987) Guanine nucleotide-binding regulatory proteins mediators of transmembrane signaling. Trends Pharmacol. Sci. 8, 478–481.CrossRefGoogle Scholar
  9. Hepler, J. R and Gilman, A. G. (1992) G proteins Trends Biochem. Sci. 17, 383–387.PubMedCrossRefGoogle Scholar
  10. Jakob, H, Beckmann, H. (1986) Prenatal development disturbances in the limbic allocortex in schizophrenics. J. Neural. Transm. 65, 303–326.PubMedCrossRefGoogle Scholar
  11. Johnstone, E. C., Crow, T J., Frith, C. D, Husband, J., and Kreel, L. (1976) Cerebral ventricular size and cognitive impairment in chronic schizophrenia Lancet ii, 924–926CrossRefGoogle Scholar
  12. Katada, T. and Ui, M. (1982) Direct modification of the membrane adenylate cyclase system by islet-activating protein due to ADP ribosylation of a membrane protein Proc. Natl. Acad. Sci. USA 79, 3129–3133PubMedCrossRefGoogle Scholar
  13. Lesch, A and Bogerts, B. (1984) The diencephalon in schizophrenia: evidence for reduced thickness of the periventricular grey matter. Eur. Arch Psychiat. Neurol Sci 234, 212–219.CrossRefGoogle Scholar
  14. Lowry, O. H., Rosebrough, N. J., Farr, A. L., and Randall, R J (1951) Protein measurement with the Folin phenol reagent. J Biol. Chem. 193, 265–275PubMedGoogle Scholar
  15. Okada, F., Crow, T J., and Roberts, G. W. (1990) G proteins (Gi, Go) in the basal ganglia of control and schizophrenic bram. J. Neural Transm (Gen Section) 79, 227–234.CrossRefGoogle Scholar
  16. Okada, F, Crow, T J, and Roberts, G W. (1991) G proteins (Gi, Go) in the medial temporal lobe in schizophrenia. Preliminary report of a neurochemical correlate of structure change J Neural. Transm (Gen Section) 84, 147–153.CrossRefGoogle Scholar
  17. Okada, F., Tokumitsu, Y, Takahashi, N., Crow, T J, and Roberts, G. W. (1994) Reduced concentrations of the α-subunit of GTP-bmding protein Go in schizophrenic brain. J Neural. Transm. (Gen. Section) 95, 95–104.CrossRefGoogle Scholar
  18. Okada, F., Murakami T., and Tokumitsu, Y. (1995) Low levels of pertussis toxin adenosine diphosphate ribosylation in the schizophrenic brain Arch Gen. Psychiatry 52, 319.PubMedGoogle Scholar
  19. Okada, F., Ito, A, Honkawa T., Tokumitsu Y., and Nomura Y. (1996) Longterm neuroleptic treatments counteract dopamine D2 agonist inhibition of adenylate cyclase but do not affect pertussis toxin ADP ribosylation in the rat brain. Neurochem. Int. 28, 161–168PubMedCrossRefGoogle Scholar
  20. Roberts, G. W. (1990) Schizophrenia, the cellular biology of a functional psychosis. Trends Neurosci. 13, 207–211PubMedCrossRefGoogle Scholar
  21. Schaffner, W. and Weissmann, C. (1973) A rapid, sensitive, and specific method for the determination of protein in dilute solution Anal Bwchem. 56, 502–514CrossRefGoogle Scholar
  22. Seeman, P., Niznik, H. B., Guan, H.-C, Booth, G, and Ulpian, C. (1989) Link between D1 and D2 dopamine receptors is reduced in schizophrenia and Huntington diseased brain Proc. Natl. Acad Sci. USA 86, 10,156–10,160.PubMedCrossRefGoogle Scholar
  23. Seeman, P, Guan, H-C, and Van Tol, H. H. M. (1993) Dopamine D4 receptors elevated in schizophrenia. Nature (Lond.) 365, 441–445.CrossRefGoogle Scholar
  24. Shelton, R. C and Weinberger, D. R. (1986) X-ray computerized tomography studies of schizophrenia a review and synthesis, in The Neurology of Schizophrenia (Nasrallah, H. A. and Weinberger, D. R., eds.), Elsevier, Amsterdam, pp. 207–250.Google Scholar
  25. Suddath, R. L, Casanoca, M. E, Goldberg, T. E., Daniel, D. G., Kelsoe, J. R., and Weinberger, D. R. (1989) Temporal lobe pathology in schizophrenia: a quantitative magnetic resonance imaging study. Am. J. Psychiatry 146, 464–472.PubMedGoogle Scholar
  26. Taubes, G. (1994) Will new dopamine receptors offer a key to schizophrenia? Science 265, 1034,1035PubMedCrossRefGoogle Scholar
  27. Wedegaertner, P. B., Wilson, P. T., and Bourne, H. R. (1995) Lipid modifications of trimeric G proteins J. Biol. Chem. 270, 503–506.PubMedCrossRefGoogle Scholar

Copyright information

© Humana Press Inc 1997

Authors and Affiliations

  • Fumihiko Okada
    • 1
  1. 1.Okada Research InstituteSapporoJapan

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