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Effect of ginkgolides on β ‐amyloid‐suppressed acetylocholine release from rat hippocampal slices
Author(s) -
Lee Tzefun,
Chen Chiehfu,
Wang Lawrence C. H.
Publication year - 2004
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.1493
Subject(s) - ginkgolides , acetylcholine , cholinergic , chemistry , amyloid (mycology) , hippocampal formation , amyloid beta , tetrodotoxin , endocrinology , medicine , biophysics , pharmacology , biochemistry , peptide , biology , ginkgo biloba , inorganic chemistry
As Ginkgo has been shown to improve age‐related memory decits and β ‐amyloid‐related peptides have been suggested to play a signicant role in memory degeneration in Alzheimer's disease, the present study was carried out to examine the effect of two major ginkgolides, A and B, on β ‐amyloid peptide‐modulated acetylcholine (ACh) release from hippocampal brain slices. Addition of β ‐amyloid fragment 25–35 (0.01–1 µM) in the superfusion medium suppressed the K + ‐evoked [ 3 H]‐ACh release from the rat hippocampal slices in a concentration‐related manner; a 40% reduction in ACh outow was observed with the highest amyloid concentration used (1 µM). Inclusion of ginkgolide B (GKB, 0.01–10 µM) caused a concentration‐related reversion of the inhibitory effect elicited by the effective concentration of β ‐amyloid (1 µM). The reversal of the β ‐amyloid‐inhibited ACh release by GKB (1 µM) was not blocked by tetrodotoxin (1 µM) indicating a direct interaction of GKB on the cholinergic nerve terminals. In contrast, addition of the same concentration range of ginkgolide A (GKA, 0.01–10 µM) had no effect on β ‐amyloid‐inhibited ACh release. These results suggest that GKB may elicit its anti‐amnesic effect by minimizing the inhibitory effect of β ‐amyloid peptides on cholinergic transmission. Copyright © 2004 John Wiley & Sons, Ltd.