Abstract: Effects of bilobalide on cerebral amino acid neurotransmission

Pharmacopsychiatry. 2003 Jun;36 Suppl 1:S84-8.  Davies JA, Johns L, Jones FA.  Department of Pharmacology, Therapeutics & Toxicology, University of Wales College of Medicine, Heath Park, Cardiff CF14 4XN, Wales, UK. daviesja8@cardiff.ac.uk

Bilobalide is one of many active constituents found in EGb 761 (definition see editorial), which is extracted from Ginkgo biloba leaves. Whilst there is good, sound evidence that bilobalide exhibits neuroprotective actions in a variety of model systems, there is currently no consensus on its mechanism of action. This present communication summarises the results we have obtained with this compound on excitatory amino acid neurotransmission in the central nervous system using both neurochemical and electrophysiological techniques. Bilobalide was shown to reduce glutamate and aspartate release elicited by both high potassium-containing artificial cerebrospinal fluid (aCSF) or veratridine from mouse cortical slices.

In addition, bilobalide had a very potent effect (IC (50) 2.7 microM) on glutamate release elicited by hypoxia/hypoglycaemia-induced release from rat cortical slices. Electrophysiologically, bilobalide also decreased the frequency of gamma-aminobutyric acid (GABA) uptake inhibitor-induced depolarisations in mouse cortical slices, an effect probably mediated by a decrease in glutamate release. No definitive conclusions can be reached concerning the mechanism of action of bilobalide, but an ability to decrease excitotoxic amino acid release, particularly glutamate, would suggest that this is a probable mechanism to account for its neuroprotective properties.

PMID: 13130394 [PubMed – indexed for MEDLINE]

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