Chronic Ethanol Intake and Synaptosomal Glutamate Binding Activity

  • E. K. Michaelis
  • M. L. Michaelis
  • W. J. Freed
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 126)


The actions of ethanol within the central nervous system (CNS) are undoubtedly multifaceted and ubiquitous. However, a large body of recent neurochemical research strongly suggests that nerve cell membranes may be one of the most significant loci for alcohol’s activity and may provide the key to understanding this agent’s dramatic effects under both acute and chronic intoxication (1,2,3,4,5). Ethanol is capable of interacting with lipid constituents of the membranes as well as with the hydrophobic regions of membrane proteins (1,2), and in this way, may alter the activity of membrane enzymes, ionophores, uptake carriers, and neurotransmitter receptors (3,4,5,6). The interaction between ethanol and any of these membrane-bound proteins could result in changes in neuronal excitability throughout the CNS. It is this potential ethanol-induced alteration in normal excitability characteristics of nerve cell membranes that has been the focus of research efforts in our laboratory.


Kainic Acid Ethanol Exposure Chronic Ethanol Ethanol Withdrawal Synaptosomal Membrane 
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.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    P. Seeman, Pharmac. Rev. 24, 583 (1972).Google Scholar
  2. 2.
    J. H. Chin and D. B. Goldstein, Science 196, 684 (1977).PubMedCrossRefGoogle Scholar
  3. 3.
    Y. Israel, H. Kalant, A. E. LeBlanc, J. C. Bernstein, and I. Salazer, J. Pharmac. exp. Ther. 174, 330 (1970).Google Scholar
  4. 4.
    K. Kuriyama and M. A. Israel, Biochem. Pharmac. 22, 219 (1973).Google Scholar
  5. 5.
    M. K. Roach, M. M. Khan, R. Coffman, R. Pennington, and D. K. Davis, Brain Res. 63, 323 (1973).PubMedCrossRefGoogle Scholar
  6. 6.
    H. Wallgren, P. Nikander, P. von Boguslawsky, and J. Linkola, Acta physiol. scand. 91, 83 (1974).PubMedCrossRefGoogle Scholar
  7. 7.
    D. B. Goldstein, J. Pharmac. exp. Ther. 186, 1 (1973).Google Scholar
  8. 8.
    W. J. Horsey and K. Akert, Q. Jl. Stud. Alcohol. 14, 363 (1953).Google Scholar
  9. 9.
    A. A. Hadji-Dimo, R. Edberg, and D. H. Ingover, Q. Jl. Stud. Alcohol. 29, 828 (1953).Google Scholar
  10. 10.
    E. K. Michaelis, M. L. Michaelis, and L. L. Boyarsky, Biochim. biophys. Acta 367, 338 (1974).PubMedCrossRefGoogle Scholar
  11. 11.
    E. K. Michaelis, Biochem. biophys. Res. Commun. 65, 1004 (1975)PubMedCrossRefGoogle Scholar
  12. 12.
    D. H. Ross, Adv. Exper. Med. Biol. 85A, 459 (1977).CrossRefGoogle Scholar
  13. 13.
    A. T. Tan, J. Neurochem. 24, 127 (1975).PubMedCrossRefGoogle Scholar
  14. 14.
    S. Haldeman and H. McLennan, Brain Res. 45, 393 (1972).PubMedCrossRefGoogle Scholar
  15. 15.
    W. A Hunt, Neuropharmac. 12, 1097 (1973).CrossRefGoogle Scholar
  16. 16.
    D. G. McQuarrie and E. Fingl, J. Pharmac. exp. Ther. 124, 264 (1958).Google Scholar
  17. 17.
    G. A. R. Johnston, D. R. Curtis, J. Davies, and R. M. McCulloch, Nature 248, 804 (1974).PubMedCrossRefGoogle Scholar
  18. 18.
    E. K. Michaelis, M. J. Mulvany, and W. J. Freed, Biochem. Pharmac. In press, (1978).Google Scholar
  19. 19.
    W. J. Freed and E. K. Michaelis, Pharmac. Biochem. Behav. 8 509 (1978).CrossRefGoogle Scholar

Copyright information

© Plenum Press, New York 1980

Authors and Affiliations

  • E. K. Michaelis
    • 1
  • M. L. Michaelis
    • 1
  • W. J. Freed
    • 2
  1. 1.Neurobiology Section, Department of Human DevelopmentUniversity of KansasLawrenceUSA
  2. 2.Laboratory of Clinical PsychopharmacologyNIMH Saint Elizabeths HospitalWashington, D.CUSA

Personalised recommendations