The acute neurotoxicity of delta-methrin is thought to be associated with the release of grutamate from synaptosomes in brain.However,the mechanism how delta-methrin enhances the glutamate release has still not been e...The acute neurotoxicity of delta-methrin is thought to be associated with the release of grutamate from synaptosomes in brain.However,the mechanism how delta-methrin enhances the glutamate release has still not been elucidated.Here we report that both carbon monoxide(CO) and the activator of protein kinase C(PKC),similarly to delta-methrin,potentiate the Ca^2+-dependent glutamate release from rat cerebral cortical synaptosomes,otherwise,the release of glutamate is inhibited by zinc proporphyrin-9(ZnPP-9) and inhibitors of PKC or of protein kinase G(PKG).In addition,the inhibitors of ZnPP-9 PKC and PKG seem to weaken the enhancement of glutamate releas caused by delta-methrin.So,we conclude that CO signal transduction pathway and PKC mediate the glutamate release from synptosomes by delta-methrin.展开更多
文摘The acute neurotoxicity of delta-methrin is thought to be associated with the release of grutamate from synaptosomes in brain.However,the mechanism how delta-methrin enhances the glutamate release has still not been elucidated.Here we report that both carbon monoxide(CO) and the activator of protein kinase C(PKC),similarly to delta-methrin,potentiate the Ca^2+-dependent glutamate release from rat cerebral cortical synaptosomes,otherwise,the release of glutamate is inhibited by zinc proporphyrin-9(ZnPP-9) and inhibitors of PKC or of protein kinase G(PKG).In addition,the inhibitors of ZnPP-9 PKC and PKG seem to weaken the enhancement of glutamate releas caused by delta-methrin.So,we conclude that CO signal transduction pathway and PKC mediate the glutamate release from synptosomes by delta-methrin.
