Summary.
This study investigated the effects of bilobalide, a constituent of Ginkgo biloba, on potassium and veratridine-induced release of glutamate and aspartate from mouse cortical slices. We also studied its effects on spontaneous and N-methyl-D-aspartate (NMDA)-induced depolarizations elicited in magnesium-free artificial cerebrospinal fluid (aCSF) as well as its effect on NO-711 (a γ-aminobutyric acid (GABA) uptake inhibitor)-induced depolarizations. Bilobalide, 100 μM significantly reduced both glutamate and aspartate release elicited by potassium or veratridine. Bilobalide (5–100 μM) also significantly reduced the frequency of NO-711 induced depolarizations, however, it had no effect on spontaneous or on NMDA-induced depolarizations at 5–200 μM. These results suggest that the neuroactive properties of bilobalide may be mediated by a reduction in excitatory amino acid neurotransmitter release.
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Received June 25, 2001 Accepted October 4, 2001
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Jones, F., Chatterjee, S. & Davies, J. Effects of bilobalide on amino acid release and electrophysiology of cortical slices. Amino Acids 22, 369–379 (2002). https://doi.org/10.1007/s007260200021
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DOI: https://doi.org/10.1007/s007260200021