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Related Experiment Videos

Chronic ethanol intake and synaptosomal glutamate binding activity

E K Michaelis, M L Michaelis, W J Freed

    Advances in Experimental Medicine and Biology
    |January 1, 1980
    PubMed
    Summary

    Chronic ethanol exposure enhances sensitivity to glutamate in the central nervous system (CNS). This increased glutamate sensitivity, particularly in nerve cell membranes, may contribute to hyperexcitability after ethanol withdrawal.

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    Area of Science:

    • Neuroscience
    • Pharmacology
    • Cell Biology

    Background:

    • Ethanol's primary site of action is increasingly understood to be the plasma membrane.
    • Ethanol affects membrane-associated proteins, including those in nerve cells.
    • L-glutamic acid is a key excitatory neurotransmitter in the CNS.

    Purpose of the Study:

    • To investigate ethanol's impact on glutamate receptor sensitivity in the CNS.
    • To explore the link between ethanol-induced changes in plasma membranes and neurotransmitter function.
    • To determine if enhanced glutamate sensitivity contributes to ethanol withdrawal symptoms.

    Main Methods:

    • Examined L-glutamate binding activity in synaptosomal membranes.
    • Measured calcium ion (Ca2+) mobilization in response to glutamate.

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  • Conducted in vivo experiments to assess glutamate sensitivity during ethanol dependence.

    • Main Results:

    • Chronic ethanol administration led to enhanced L-glutamate binding and Ca2+ mobilization.
    • These effects showed an increased maximum response without significant changes in L-glutamate binding affinity (KD).
    • In vivo studies revealed glutamate sensitization during ethanol dependence.

    Conclusions:

    • Ethanol exposure, particularly chronic administration, sensitizes the CNS to L-glutamate.
    • This sensitization, mediated by plasma membrane effects, may be a causal factor in post-withdrawal CNS hyperexcitability.
    • Findings highlight the role of membrane-bound neurotransmitter receptors in ethanol's neurobiological effects.