Abstract
Conclusion
Under ordinary circumstances systemically administered γ-amino butyric acid does not produce electrophysiological effects. Following destruction of the blood-brain barrier the synaptic actions are similar to those produced by topical application. In regions of increased barrier-permeability, intravenous GABA abolishes or reduces the frequency of spontaneous paroxysmal discharges arising from such areas. Therefore systemically administered GABA produces no synaptic effects because of failure to penetrate the blood-brain barrier. By permitting rapid exchanges of GABA between blood and brain during electrophysiological studies following barrier lesions, information was obtained relating to the role of γ-amino butyric acid in the central nervous system not attainable by the method of topical application. Production of experimental, localized regions of blood-brain barrier loss may have applications for the study of substances that are otherwise denied access to the cells of the central nervous system.
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