Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Letter
  • Published:

Increased concentrations and lateral asymmetry of amygdala dopamine in schizophrenia

Abstract

There is a growing body of evidence in support of the view of schizophrenia as a dysfunction of the left temporal lobe. This hypothesis, first proposed by Flor-Henry1, stemmed from the frequently observed association of schizophreniform psychoses with left-sided temporal lobe epilepsy. As yet the evidence is solely clinical, with a wide range of psychological and physiological measurements indicating a left hemisphere disorder in patients with schizophrenia2–4. It is not, however, inconsistent with the major neurochemical hypothesis of schizophrenia, which proposes an increase in dopaminergic neurotransmission which can be blocked by neuroleptic drugs. One region of the medial temporal lobe, the amygdala, receives a major dopaminergic innervation from the ventral tegmental area5. In fact this meso-limbic dopaminergic tract, which also innervates the nucleus accumbens and olfactory tubercule, has been implicated in psychosis and in antipsychotic drug action6,7. We have attempted here to test whether there is a neurochemical correlate of the Flor-Henry hypothesis using brain tissue collected post mortem from schizophrenic patients and controls. The results indicate that a specific increase of dopamine is found in the amygdalae in the left cerebral hemisphere of the schizophrenic group.

This is a preview of subscription content, access via your institution

Access options

Rent or buy this article

Prices vary by article type

from$1.95

to$39.95

Prices may be subject to local taxes which are calculated during checkout

Similar content being viewed by others

References

  1. Flor-Henry, P. Epilepsia 10, 363–395 (1969).

    Article  CAS  Google Scholar 

  2. Gruzelier, J. H. Psychol. Med. 11, 219–227 (1981).

    Article  CAS  Google Scholar 

  3. Newlin, D. B., Carpenter, B. & Golden, C. J. Biol. Psychiatr. 16, 561–589 (1981).

    CAS  Google Scholar 

  4. Merrin, E. L. Compreh. Psychiatr. 23, 55–67 (1982).

    Article  CAS  Google Scholar 

  5. Dahlstrom, A. & Fuxe, K. Acta physiol. scand. Suppl. 232, 1–55 (1964).

    Google Scholar 

  6. Stevens, J. R. Arch. gen. Psychiatr. 29, 177–189 (1973).

    Article  CAS  Google Scholar 

  7. Hornykiewiecz, O. Neurosciences 3, 773–783 (1978).

    Article  Google Scholar 

  8. Ungerstedt, U. Acta physiol. scand. Suppl. 367, 69–93 (1971).

    Article  CAS  Google Scholar 

  9. Barolin, G. S., Bernheimer, H. & Hornykiewicz, O. Schweiz. Arch. Neurol. Psychiatr. 94, 241–243 (1964).

    Google Scholar 

  10. Yamamoto, B. K. & Freed, C. R. Nature 298, 467–468 (1982).

    Article  ADS  CAS  Google Scholar 

  11. Slopsema, J. S., van der Gugten, J. & de Bruin, J. P. C. Brain Res. 250, 197–200 (1982).

    Article  CAS  Google Scholar 

  12. Glick, S. D. & Ross, D. A. Trends Neurosci. 4, 196–199 (1981).

    Article  Google Scholar 

  13. Glick, S. D., Ross, D. A. & Hough, L. D. Brain Res. 234, 53–63 (1982).

    Article  CAS  Google Scholar 

  14. Oke, A., Keller, R., Mefford, I. & Adams, R. Science 200, 1411–1413 (1978).

    Article  ADS  CAS  Google Scholar 

  15. Bird, E. D., Spokes, E. G. S. & Iversen, L. L. Brain 102, 347–360 (1979).

    Article  CAS  Google Scholar 

  16. Hornykiewicz, O. Nature 299, 484–486 (1982).

    Article  ADS  CAS  Google Scholar 

  17. Rossor, M., Garrett, N. & Iversen, L. L. J. Neurochem. 35, 743–745 (1980).

    Article  CAS  Google Scholar 

  18. Spokes, E. G. S. Brain 102, 333–346 (1979).

    Article  CAS  Google Scholar 

  19. Mackay, A. V. P. et al. Arch. gen. Psychiatr. 39, 991–997 (1982).

    Article  CAS  Google Scholar 

  20. Crow, T. J. et al. in Transmitter Biochemistry of Human Brain Tissue (eds Riederer P. & Usdin, E.) (Macmillan, London, 1981).

    Google Scholar 

  21. Trimble, M. R. & Perez, M. M. in Temporal Lobe Epilepsy, Mania, and Schizophrenia and the Limbic System (eds Koella, W. P. & Trimble, M. R.) 98–105 (Karger, Basle, 1982).

    Google Scholar 

  22. Post, R. M., Unde, T. W., Ballenger, J. C. & Bunney, W. E. in Temporal Lobe Epilepsy, Mania, and Schizophrenia and the Limbic System (eds Koella, W. P. & Trimble, M. R.) 117–156 (Karger, Basle, 1982).

    Google Scholar 

  23. Stevens, J. R. & Livermore, A. Neurology 28, 36–46 (1978).

    Article  CAS  Google Scholar 

  24. Gruzelier, J. H. & Hammond, N. V. Stud. psychologica 19, 40–50 (1977).

    Google Scholar 

  25. Tomer, R., Mintz, M. & Myslebodsky, M. S. Psychopharmacology 77, 168–170 (1982).

    Article  CAS  Google Scholar 

  26. Waziri, R. Psychopharmacology 68, 51–53 (1980).

    Article  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Rights and permissions

Reprints and permissions

About this article

Cite this article

Reynolds, G. Increased concentrations and lateral asymmetry of amygdala dopamine in schizophrenia. Nature 305, 527–529 (1983). https://doi.org/10.1038/305527a0

Download citation

  • Received:

  • Accepted:

  • Issue Date:

  • DOI: https://doi.org/10.1038/305527a0

This article is cited by

Comments

By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.

Search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing