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:

Direct evidence for presynaptic and postsynaptic dopamine receptors in brain

Abstract

CENTRAL dopamine (DA)-containing neurones are thought to be involved in several human diseases including Parkinson's disease and schizophrenia, and to act as sites of action of some drugs of abuse. One of these DA systems, the nigrostriatal projection (NSP), has its origin in the substantia nigra (SN), pars compacta and innervates the caudate-putamen (CP). In the SN the dendritic processes of DA neurones have been shown to contain DA and vesicles1–3 and there is evidence that DA can be released by cells in the SN4–6. It has therefore been proposed that one mechanism by which the activity of DA neurones is regulated is through the action of dendritically released DA on hypothesised ‘autoreceptors’ on DA perikarya or dendrites7–9. Recently, however, this view has been challenged by the observation that DA-sensitive adenylate cyclase, an enzyme thought to be coupled with the DA receptor10, is located on terminals of the striatonigral or pallidonigral projection11,12 rather than on the DA cells themselves13–15. Similarly, in the CP where the existence of autoreceptors on DA terminals has been suggested16, the DA-sensitive adenylate cyclase has been shown to be localised on postsynaptic structures rather than on the DA terminals17,18. An established method for studying the DA receptor involves measuring DA receptor binding with labelled DA agonists or antagonists19,20. To further elucidate the location of DA receptors in the SN and CP, we have examined the effects of selective lesions of the NSP on labelling of DA receptors in these structures. These lesions, which are placed in the axons of the NSP, are known to cause near-complete anterograde and retrograde degeneration of the terminals and cell bodies of this system21. The advantage of this lesion technique over previous approaches is that it avoids nonspecific damage of the areas studied. Our results provide direct evidence of presynaptic and postsynaptic dopamine receptors in rat brain.

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

Access options

Buy this article

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

Similar content being viewed by others

References

  1. Hajdu, F., Hassler, R. & Bak, I. J. Z. Zellforsch. 146, 207–221 (1973).

    Article  CAS  Google Scholar 

  2. Bjorklund, A. & Lindvall, O. Brain Res. 83, 531–537 (1975).

    Article  CAS  Google Scholar 

  3. Parizek, J., Hassler, R. & Bak, I. J. Z. Zellforsch. 115, 137–148 (1971).

    Article  Google Scholar 

  4. Geffen, L. B., Jessell, T. M., Cuello, A. C. & Iversen, L. L. Nature 260, 258–260 (1976).

    Article  ADS  CAS  Google Scholar 

  5. Korf, J., Zieleman, M. & Westerink, B. H. C. Nature 260, 257–258 (1976).

    Article  ADS  CAS  Google Scholar 

  6. Nieoullon, A., Cheramy, A. & Glowinski, J. Nature 266, 375–377 (1977).

    Article  ADS  CAS  Google Scholar 

  7. Aghajanian, G. K. & Bunney, B. S. in Frontiers in Neurology and Neuroscience Research (eds Seeman, P. & Brown, G. M.) 4–11 (University of Toronto Press, 1974).

    Google Scholar 

  8. Groves, P. M., Wilson, C. J., Young, S. J. & Rebec, G. U. Science 190, 522–529 (1975).

    Article  ADS  CAS  Google Scholar 

  9. Bunney, B. S. & Aghajanian, G. K. in Pre- and Postsynaptic Receptors (eds Usdin, E. & Bunney, W. E.) 89–122 (Dekker, New York, 1975).

    Google Scholar 

  10. Kebabian, J. W., Petzold, G. L. & Greengard, P. Proc. natn. Acad. Sci. U.S.A. 69, 2145–2149 (1972).

    Article  ADS  CAS  Google Scholar 

  11. Gale, K., Guidotti, A. & Costa, E. Science 195, 503–505 (1977).

    Article  ADS  CAS  Google Scholar 

  12. Spano, P. F., Trabucchi, M. & DiChiara, G. Science 196, 1343–1345 (1977).

    Article  ADS  CAS  Google Scholar 

  13. Kebabian, J. W. & Saavedra, J. M. Science 193, 683–685 (1976).

    Article  ADS  CAS  Google Scholar 

  14. Phillipson, O. T., Emson, P. C., Horn, A. S. & Jessell, T. Brain Res. 136, 45–58 (1977).

    Article  CAS  Google Scholar 

  15. Spano, P. F., DiChiara, G., Tonon, G. C. & Trabucchi, M. J. Neurochem. 27, 1565–1568 (1976).

    Article  CAS  Google Scholar 

  16. Kehr, W., Carlsson, A., Lindqvist, M., Magnusson, T. & Atack, C. V. J. Pharm. Pharmac. 24, 744–747 (1972).

    Article  CAS  Google Scholar 

  17. Schwarcz, R. & Coyle, J. T. Brain Res. 127, 235–249 (1977).

    Article  CAS  Google Scholar 

  18. McGeer, E. G., Innanen, V. T. & McGeer, P. L. Brain Res. 118, 356–357 (1976).

    Article  CAS  Google Scholar 

  19. Seeman, P., Lee, T., Chau-Wong, M., Tedesco, J. & Wong, K. Proc. natn. Acad. Sci. U.S.A. 73, 4354–4358 (1976).

    Article  ADS  CAS  Google Scholar 

  20. Burt, D. R., Enna, S. J., Creese, I. & Snyder, S. Proc. natn. Acad. U.S.A. 72, 4655–4659 (1975).

    Article  ADS  CAS  Google Scholar 

  21. Clavier, R. M. & Fibiger, H. C. Brain Res. 131, 271–286 (1977).

    Article  CAS  Google Scholar 

  22. Fibiger, H. C., McGeer, E. G. & Atmadja, S. J. Neurochem. 21, 373–385 (1973).

    Article  CAS  Google Scholar 

  23. McGeer, E. G., Gibson, S. & McGeer, P. L. Can. J. Biochem. 45, 1557–1563 (1967).

    Article  CAS  Google Scholar 

  24. Chalmers, A., McGeer, E. G., Wickson, V. & McGeer, P. L. Comp. gen. Pharmac. 1, 385–390 (1970).

    Article  CAS  Google Scholar 

  25. Hattori, T., Fibiger, H. C. & McGeer, P. L. J. comp. Neurol. 162, 487–504 (1975).

    Article  CAS  Google Scholar 

  26. Leysen, J. E., Gommersen, W. & Laduron, P. M. Biochem. Pharmac. 27, 307–316 (1978).

    Article  CAS  Google Scholar 

  27. Ungerstedt, U. Acta physiol. scand. 82, suppl. 367 69–93 (1971).

    Article  Google Scholar 

  28. Price, M. T. C. & Fibiger, H. C. Eur. J. Pharmac. 29, 249–252 (1974).

    Article  CAS  Google Scholar 

  29. Christensen, A. V., Fjalland, B. & Moller-Nielsen, J. Psychopharmacology 48, 1–12 (1976).

    Article  CAS  Google Scholar 

  30. Muller, P. & Seeman, P. Life Sci. 21, 1751–1758 (1977).

    Article  CAS  Google Scholar 

  31. Burt, D. R., Creese, I. & Snyder, S. H. Science 196, 326–328 (1977).

    Article  ADS  CAS  Google Scholar 

  32. Creese, I., Burt, D. R. & Snyder, S. H. Science 197, 596–598 (1977).

    Article  ADS  CAS  Google Scholar 

  33. DiChiara, G., Porceddu, M. L., Spano, P. F. & Gessa, G. L. Brain Res. 130, 374–382 (1977).

    Article  CAS  Google Scholar 

  34. Iversen, L. L., Rogawski, M. A. & Miller, R. J. Molec. Pharmac. 12, 251–262 (1976).

    CAS  Google Scholar 

  35. Christiansen, J. & Squires, R. F. J. Pharm. Pharmac. 26, 367–369 (1974).

    Article  CAS  Google Scholar 

  36. Carlsson, A. in Pre- and Postsynaptic Receptors (eds Usdin, E. & Bunney, W. E.) 49–65 (Dekker, New York, 1975).

    Google Scholar 

  37. Strombom, U. Acta physiol. scand., Suppl. 431 (1975).

  38. Creese, I., Burt, D. R. & Snyder, S. H. Life Sci. 17, 993–1002 (1975).

    Article  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Rights and permissions

Reprints and permissions

About this article

Cite this article

NAGY, J., LEE, T., SEEMAN, P. et al. Direct evidence for presynaptic and postsynaptic dopamine receptors in brain. Nature 274, 278–281 (1978). https://doi.org/10.1038/274278a0

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue date:

  • DOI: https://doi.org/10.1038/274278a0

This article is cited by

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