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Regulation of GABAA Currents by Excitatory Amino Acids

  • Armin Stelzer
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 268)

Abstract

In the mammalian cortex, glutamate (1) amd γ-aminobutyric acid (GABA) (2) are the principal transmitters mediating excitatory and inhibitory synaptic events. Glutamate activates cation conductances that lead to membrane depolarization. This action is mediated by at least three distinct receptor subtypes defined by their main agonists as N-methyl-D-aspartate (NMDA), quisqualate and kainate receptors (1). GABA controls at least two conductances that produce hyperpolarization in cortical neurons: an early inhibitory synaptic potential mediated by chloride currents through GABAA receptors (2) and a late hyperpolarization mediated by potassium current through GABAB receptors (3).

Keywords

GABAA Receptor Excitatory Amino Acid Calcium Current Chloride Current Bath Application 
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.

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References

  1. 1.
    Watkins, J.C. & Evans, R.H., Ann. Rev. Pharmacol. Tox. 21 165–204 (1981).CrossRefGoogle Scholar
  2. 2.
    Krnjevic, K., Physiol.Rev. 54, 418–540 (1974).Google Scholar
  3. 3.
    Nicoll, R.A. & Alger, B.E. Science 212, 957–959 (1981).PubMedCrossRefGoogle Scholar
  4. 4.
    Stelzer, A., Slater, N.T. & ten Bruggencate, G., Nature 326, 698–701 (1987).PubMedCrossRefGoogle Scholar
  5. 5.
    Stelzer, A. & Wong, R.K.S., Nature 337, 170–173 (1989).PubMedCrossRefGoogle Scholar
  6. 6.
    Slater, N.T., Stelzer, A., Galvan, M., Neurosci. Lett. 60, 25–31 (1985).PubMedCrossRefGoogle Scholar
  7. 7.
    Stasheff, S.F., Bragdon, A.C. & Wilson, W.A., Brain Res. 344, 296–302 (1985).PubMedCrossRefGoogle Scholar
  8. 8.
    MacDermott, A.B., Mayer, M.L, Westbrook, G.L., Smith, S.J. & Barker, J.L., Nature 321, 519–522 (1986).PubMedCrossRefGoogle Scholar
  9. 9.
    Krnjevic, K, Morris, M.E. & Ropert, N., Brain Res. 374,1–11 (1986).PubMedCrossRefGoogle Scholar
  10. 10.
    Stelzer, A., Kay, A.R. & Wong, R.K.S., Science 241, 339–341 (1988).PubMedCrossRefGoogle Scholar
  11. 11.
    Chen, Q.X., Kay, A.R., Stelzer, A. & Wong, R.K.S., J. Physiol. (in press).Google Scholar
  12. 12.
    Olsen, R.W. & Venter, J.C., (eds.) Benzodiazepine/GABA Receptors and Chloride Channels: Structural and Functional Properties (Liss, New York, 1987).Google Scholar
  13. 13.
    Kay, A.R. & Wong, R.K.S., J. Neurosci. Meth. 16, 227–238 (1986).CrossRefGoogle Scholar
  14. 14.
    Hamill, O.P., Marty, A., Neher, E., Sakmann, B. & Sigworth, F.J., Pfluegers Arch. ges. Physiol. 391, 85–100 (1981).CrossRefGoogle Scholar
  15. 15.
    Kiskin, N.I., Krishtal, O.A. & Tsyndrenko, A.Y., Neurosci. Lett. 63, 225–230 (1986).PubMedCrossRefGoogle Scholar
  16. 16.
    Stelzer, A. & Wong, R.K.S., Soc. Neurosci. Abstr. 369.2 (1988).Google Scholar
  17. 17.
    Sigel, E. & Baur, R., Proc. Natl. Acad.Sci. USA 86,2938–2942 (1988).Google Scholar
  18. 18.
    Browning et al., Soc. Neurosci. Abstr. (1989).Google Scholar
  19. 19.
    Nishizuka, Y., Science 233, 305–312 (1986).PubMedCrossRefGoogle Scholar
  20. 20.
    Kaibuchi, K. et al., Cell Calcium 3, 323 (1982).PubMedCrossRefGoogle Scholar
  21. 21.
    Castagna, M. et al., J. Biol. Chem. 257, 7847 (1982).PubMedGoogle Scholar
  22. 22.
    Doerner, D., Pitler, T.A. & Alger, B.E., J. Neurosci. 8(11), 4069–4078 (1988).PubMedGoogle Scholar
  23. 23.
    Ferraro, T.N. & Hare, T.A., Brain Res. 338, 53–60 (1985).PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 1990

Authors and Affiliations

  • Armin Stelzer
    • 1
  1. 1.Department of Neurology, College of Physicians and Surgeons, 4-408Columbia UniversityNew YorkUSA

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