The neurotoxicity of zinc, released from nerve terminals during global ischemia, may contribute to the delayed death of certain selectively vulnerable neuronal populations. A likely first event in zinc-induced neuronal death appears to be its permeation across the plasma membrane, largely through voltage-and agonist-gated calcium channels. Considering the possibility that cellular Zn2+ overload might be lethal for reasons similar to cellular calcium overload, we tested the hypothesis that Zn2+ neurotoxicity might be ... .

Another facet of nitric oxide: reduction of toxic zinc influx through voltage-gated channels

Canzoniero L. M.;
1991

Abstract

The neurotoxicity of zinc, released from nerve terminals during global ischemia, may contribute to the delayed death of certain selectively vulnerable neuronal populations. A likely first event in zinc-induced neuronal death appears to be its permeation across the plasma membrane, largely through voltage-and agonist-gated calcium channels. Considering the possibility that cellular Zn2+ overload might be lethal for reasons similar to cellular calcium overload, we tested the hypothesis that Zn2+ neurotoxicity might be ... .
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/20.500.12070/8708
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