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GluR6-containing KA receptor mediates the activation of p38 MAP kinase in rat hippocampal CA1 region during brain ischemia injury by Juan Chen; Chong Li; Dong-Sheng Pei; Dong Han; Xiao-Mei Liu; Hai-Xia Jiang; Xiao-Tian Wang; Qiu-Hua Guan; Xiang-Ru Wen; Xiao-Yu Hou; Guang-Yi Zhang is a Neuroscience article available to read on EtoBox.

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## Abstract Our previous study showed that kainate (KA) receptor subunit GluR6 played an important role in ischemia‐induced MLK3 and JNK activation and neuronal degeneration through the GluR6‐PSD95‐MLK3 signaling module. However, whether the KA receptors subunit GluR6 is involved in the activation of p38 MAP kinase during the transient brain ischemia/reperfusion (I/R) in the rat hippocampal CA1 subfield is still unknown. In this present study, we first evaluated the time‐course of phospho‐p38 MAP kinase at various time‐points after 15 min of ischemia and then observed the effects of antagonist of KA receptor subunit GluR6, GluR6 antisence oligodeoxynucleotides on the phosphorylation of p38 MAP kinase induced by I/R. Results showed that inhibiting KA receptor GluR6 or suppressing the expression of KA receptor GluR6 could down‐regulate the elevation of phospho‐p38 MAP kinase induced by I/R. These drugs also reduced the phosphorylation of MLK3, MKK3/MKK6, MKK4, and MAPKAPK2. Additionally, our results indicated administration of three drugs, including p38 MAP kinase inhibitor before brain ischemia significantly decreased the number of TUNEL‐positive cells detected at 3 days of reperfus

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Author

Juan Chen; Chong Li; Dong-Sheng Pei; Dong Han; Xiao-Mei Liu; Hai-Xia Jiang; Xiao-Tian Wang; Qiu-Hua Guan; Xiang-Ru Wen; Xiao-Yu Hou; Guang-Yi Zhang

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley (ISSN 1050-9631)

Published

2008

Language

EN

Field

Neuroscience (Life Sciences)