Abeta(25-35) and Abeta(1-40) act on different calcium channels in CA1 hippocampal neurons

The acute effects of beta-amyloid (25-35) and (1-40) on high voltage activated calcium channels were compared in CA1 pyramidal cells of adult mouse hippocampal slices using the whole-cell patch-clamp recording. Bath application of oligomeric beta-amyloid (25-35) reversibly increased the barium curre...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2002-09, Vol.296 (5), p.1317
Main Authors: Rovira, Catherine, Arbez, Nicolas, Mariani, Jean
Format: Article
Language:English
Subjects:
Amyloid beta-Peptides - antagonists & inhibitors
Amyloid beta-Peptides - pharmacology
Animals
Barium - metabolism
Calcium Channel Blockers - pharmacology
Calcium Channels - physiology
Calcium Channels, L-Type - physiology
Cells, Cultured
Electric Conductivity
Hippocampus - cytology
Kinetics
Mice
Nifedipine - pharmacology
Peptide Fragments - antagonists & inhibitors
Peptide Fragments - pharmacology
Pyramidal Cells - drug effects
Pyramidal Cells - physiology
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Summary:The acute effects of beta-amyloid (25-35) and (1-40) on high voltage activated calcium channels were compared in CA1 pyramidal cells of adult mouse hippocampal slices using the whole-cell patch-clamp recording. Bath application of oligomeric beta-amyloid (25-35) reversibly increased the barium current (I(Ba)) to 1.61 (normalized amplitude), while oligomeric beta-amyloid (1-40) reversibly enhanced the I(Ba) to 1.74. Reverse-sequence beta-amyloid [(35-25) and (40-1)] had no effect. The effect of beta-amyloid (25-35) was blocked by nifedipine, a selective antagonist of L-type calcium channels. In contrast, the effect of beta-amyloid (1-40) was not blocked by nifedipine and I(Ba) was enhanced to 4.96. It is concluded that these oligomeric peptides may act through different types of calcium channels and/or receptors. The toxicity of Abeta(25-35) implicates a potentiation of L-type calcium channels while the one of Abeta(1-40) is related to an increase of non-L-type calcium channels, which may involve an increase in transmitter release.
ISSN:0006-291X