Premium
Rapid Communication: Ca 2+ Channel Blockers Attenuate β‐Amyloid Peptide Toxicity to Cortical Neurons in Culture
Author(s) -
Weiss John H.,
Pike Christian J.,
Cotman Carl W.
Publication year - 1994
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1994.62010372.x
Subject(s) - neurotoxicity , neurodegeneration , nimodipine , beta (programming language) , glutamate receptor , pharmacology , chemistry , channel blocker , neuroscience , toxicity , receptor , medicine , biology , biochemistry , calcium , disease , computer science , programming language
Deposit of β‐amyloid protein (Aβ) in Alzheimer's disease brain may contribute to the associated neurodegeneration. We have studied the neurotoxicity of Aβ in primary cultures of murine cortical neurons, with the aim of identifying pharmacologic ways of attenuating the injury. Exposure of cultures to Aβ (25–35 fragment; 3–25 4mU M ) generally triggers slow, concentration‐dependent neurodegeneration (over 24–72 h). With submaximal Aβ‐ (25–35) exposure (10 μ M ), substantial (>40% within 48 h) degeneration often occurs and is markedly attenuated by the presence of the Ca 2+ channel blockers nimodipine (1–20 μ M ) and Co 2+ (100 μ M ) during the Aβ exposure. However, Aβ neurotoxicity is not affected by the presence of glutamate receptor antagonists. We suggest that Ca 2+ influx through voltage‐gated Ca 2+ channels may contribute to Aβ‐induced neuronal injury and that nimodipine and Co 2+ , by attenuating such influx, are able to attenuate Aβ neurotoxicity.