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Related Experiment Videos

Inhibitory, GABAergic nerve terminals decrease at sites of focal epilepsy.

C E Ribak, A B Harris, J E Vaughn

    Science (New York, N.Y.)
    |July 13, 1979
    PubMed
    Summary
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    Epilepsy in monkeys shows a significant decrease in gamma-aminobutyric acid (GABA) nerve terminals in seizure areas. This loss of GABAergic inhibition may cause epileptic activity in cortical neurons.

    Area of Science:

    • Neuroscience
    • Neurochemistry

    Background:

    • Gamma-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the mammalian central nervous system.
    • Glutamic acid decarboxylase (GAD) is the enzyme responsible for synthesizing GABA.

    Purpose of the Study:

    • To investigate the distribution of GABAergic nerve terminals in the sensorimotor cortex of normal and epileptic monkeys.
    • To determine if there are changes in GABAergic terminals at seizure foci.

    Main Methods:

    • Immunocytochemistry was used to localize GAD-positive nerve terminals.
    • Ultrastructural analysis was performed on nerve terminals.
    • Monkeys were induced into an epileptic state using alumina gel application to the cortex.

    Main Results:

    Related Experiment Videos

    • GABAergic nerve terminals were found throughout all layers of the normal monkey sensorimotor cortex.
    • These terminals appeared to originate from aspinous and sparsely spinous stellate neurons.
    • A significant numerical decrease in GAD-positive nerve terminals was observed at seizure foci in epileptic monkeys.

    Conclusions:

    • The study indicates a functional loss of GABAergic inhibitory synapses at seizure foci in epileptic monkeys.
    • This loss of inhibition could contribute to the epileptic activity observed in cortical pyramidal neurons.