Neurochemical Research

, Volume 11, Issue 11, pp 1533–1545 | Cite as

Functional and biochemical characteristics of a putative quisqualate-type receptor in rat striatum: Effect of brain lesions

  • Maria Isolde Rudolph
  • Gonzalo Bustos
Original Articles


Excitatory amino acids such asl-glutamate (Glu) and quisqualate (QUIS) markedly potentiated K+-evoked release of exogeneous [3H]dopamine (DA) from rat striatal slices. Intranstriatal kainic acid injections resulted in a total disappearance of the stimulatory effects of Glu on evoked-release of [3H]DA as well as in a parallel reduction in the maximal number (Bmax) of ad-aspartate-insensitivel-[3H]Glu binding site in striatal particulate fractions. Following cortical ablation, the potentiating effect of Glu on [3H]DA release in decorticated striatal slices lasted longer, compared to normal slices, and occured during the 2nd min following K+-depolarization. However, the extent (%) of Glu stimulation on [3H]DA release remained the same in decorticated and normal striatal slices. Cortical ablation produced also a significant decrease in the Bmax and in theK d′ of thed-aspartateinsensitive binding site towardsl[3H]Glu. These results support the proposal that thed-aspartate-insensitive Glu binding site is somehow related to an amino acid receptor-mediated modulation of dopaminergic transmission in the rat corpus striatum.


Dopamine Particulate Fraction Excitatory Amino Acid Kainic Acid Corpus Striatum 
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  1. 1.
    Giorguieff, M. F., Kemel, M. L., andGlowinski, J. 1977. Presynaptic effects ofl-glutamic acid on the release of dopamine in rat striatal slices. Neurosci. Lett. 6:73–77.Google Scholar
  2. 2.
    Roberts, P. J., andAnderson, J. D. 1979. Stimulatory effects ofl-glutamate and related acid on [3H]dopamine release from rat striatum: an in vitro model for glutamate actions. J. Neurochem. 32:1539–1545.Google Scholar
  3. 3.
    Rudolph, M. I., Arqueros, L., andBustos, G. 1983.l-glutamic acid, a neuromodulator of synaptic transmission in the rat corpus striatum.. Neurochem. Intern. 5:479–486.Google Scholar
  4. 4.
    Rudolph, M. I., andBustos, G. Search of al-glutamate receptor related to modulation of neurotransmission in the rat corpus striatum. Neurochem Intern (in press).Google Scholar
  5. 5.
    Schwarcz, R., andCoyle, J. T. 1977. Striatal lesions with kainic acid: neurochemical characteristics. Brain Res. 127:235–249.Google Scholar
  6. 6.
    Fagg, G. E., andFoster, A. C. 1983. Amino acid neurotransmitters and their pathways in the mammalian central nervous system. Neuroscience 9:701–719.Google Scholar
  7. 7.
    Fonnum, F. 1984. Glutamate: a neurotransmitter in the mammalian brain. J. Neurochem. 42:1–11.Google Scholar
  8. 8.
    Rudolph, M. I., andBustos, G. 1981. Participation of striatal intrinsic neurons on the effect ofl-glutamic acid upon dopamine release. Arch. Biol. Med. Exp. 14:294.Google Scholar
  9. 9.
    Rudolph, M. I., andBustos, G. 1983. Characterization of al-glutamate receptor in the rat corpus striatum. Arch. Biol. Med. Exp. 16:R-116.Google Scholar
  10. 10.
    McGeer, P. L., McGeer, E. G., Scherer, U., andSingh, K. 1977. A glutamatergic corticostriatal path? Brain Res. 128:369–373.Google Scholar
  11. 11.
    Arqueros, L., Abarca, J., andBustos, G. 1985. Release ofd-[3H]aspartic acid from the rat striatum. Effect of veratridine-evoked depolarization, fronto-parietal cortex ablation and striatal lesions with kainic acid. Biochem. Pharmacol. 34:1217–1224.Google Scholar
  12. 12.
    Schrier, B. R., andShuster, L. 1967. A simplified radiochemical assay for choline acetyltransferase. J. Neurochem. 14:977–985.Google Scholar
  13. 13.
    Laverty, R., andTaylor, K. M. 1968. The fluorometric assay of catecholamines and related compounds. Anal. Biochem. 22:269–279.Google Scholar
  14. 14.
    Bustos, G., andRoth, R. H. 1972. Release of monoamines from the striatum and hypothalamus effect of γ-hydroxybutyrate. Brit. J. Pharmacol. 46:101–115.Google Scholar
  15. 15.
    Lowry, O. H., Rosebrough, N. S., Farr, A.-L., andRandall, R. J. 1951. Protein measurement with the Folin phenol reagent. J. Biol. Chem. 193:265–275.Google Scholar
  16. 16.
    Scatchard, G. 1949. The attractions of proteins for small molecules and ions. Ann. New York Acad. Sci. 51:660–672.Google Scholar
  17. 17.
    Bennett Jr., J. P. 1978. Methods in binding studies, Pages 57–90,in Yamamura, H. I., Enna, S. J., andKuhar, M. J. (eds.). Neurotransmitter receptor binding. Raven Press, New York.Google Scholar
  18. 18.
    Watkins, J. C., andEvans, R. H. 1981. Excitatory amino acid transmitter. Ann. Rev. Pharmacol. Toxicol. 21:165–204.Google Scholar
  19. 19.
    Mc. Lennan, H. 1981. Excitatory amino acid receptor, Pages 215–220,in,Lombardini,J. B. andKenny,A. D. (eds.) The role of peptides and amino acids as neurotransmitter, Alan R. Liss, New York.Google Scholar
  20. 20.
    Monaghan, D. T., Yao, D., andCotman, C. W. 1985.l-[3H]Glutamate binds to kainate-NMDA-and AMPA-sensitive binding sites: an autoradiographic analysis. Brain Res. 340:378–383.Google Scholar
  21. 21.
    Robinson, M. B., Crooks, S. L., Johnson, R. L., andKoerner, J. F. 1985. Displacement ofDl-[3H]-2-amino-4-phosphonobutanoic Acid binding with methyl-substituted APB analogues and glutamate agonists. Biochemistry 24:2401–2405.Google Scholar
  22. 22.
    Kitai, S. T., Kocsis, J. D., Preston, R. J., andSugimori, M. 1976. Monosynaptic inputs to caudate neurons identified by intracellular injection of horseradish peroxidase. Brain Res. 109:601–606.Google Scholar
  23. 23.
    Hattori, T., andFibiger, H. C. 1982. On the use of lesions of afferents to localize neurotransmitter receptor sites in the striatum.. Brain Res. 238:245–250.Google Scholar
  24. 24.
    Pinching, A. J., andPowell, T. P. S. 1971. Ultra-structural features of transneuronal cell degeneration in the olfactory system J. Cell Sci. 8:253–268.Google Scholar
  25. 25.
    Ghetti, B., andWisniewsky, H. M. 1972. On degeneration of terminals in, the cat striate cortex. Brain Res. 44:630–635.Google Scholar
  26. 26.
    Ghetti, B., Horoupian, D. S., andWisniewsky, H. M. 1972. Transsynaptic response of the lateral geniculate nucleus and the pattern of degeneration of the nerve terminals in the rhesus monkey after eye enucleation. Brain Res. 45:31–48.Google Scholar
  27. 27.
    Roberts, P. J., Mc. Bean, J. G., Sharif, N. A., andThoma, E. M. 1982. Striatal glutamatergic function: modifications following specific, lesions. Brain Res. 235:83–91.Google Scholar
  28. 28.
    Biziere, K. Thompson, H., andCoyle, J. T. 1980. Characterization of specific, highaffinity binding sites forl-[3H]glutamic acid in rat brain membranes. Brain Res. 183:421–433.Google Scholar
  29. 29.
    Mc Lennan, H. 1980. The effect of decortication on the excitatory amino acid sensitivity of striatal neurons. 18:313–316.Google Scholar

Copyright information

© Plenum Publishing Corporation 1986

Authors and Affiliations

  • Maria Isolde Rudolph
    • 1
  • Gonzalo Bustos
    • 1
  1. 1.Laboratory of Biochemical Pharmacology Department of Cell BiologyPontificia Universidad Católica de ChileSantiagoChile

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