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Functional cooperation between KA2 and GluR6 subunits is involved in the ischemic brain injury
Author(s) -
Jiang HaiXia,
Guan QiuHua,
Pei DongSheng,
Zhang GuangYi
Publication year - 2007
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.21334
Subject(s) - protein subunit , ischemia , signal transduction , chemistry , phosphorylation , neuroscience , pharmacology , microbiology and biotechnology , medicine , biology , biochemistry , gene
We investigated the possible relationships between KA2 subunit and GluR6 subunit, as well as the role of KA2 subunit in neuronal death induced by cerebral ischemia/reperfusion. Our results indicated that intracerebroventricular infusion of KA2 antisense oligodeoxynucleotides (AS) not only knocked down the expressions of KA2 and GluR6, but also suppressed the assembly of the GluR6/KA2‐PSD95‐MLK3 signaling module, and inhibited JNK activation and phosphorylation of c‐jun. In addition, infusion of KA2 AS increased neuronal survival in CA1 region after 5 days of reperfusion. More interestingly, we found that the combination of KA2 and GluR6 AS exerted more significant effects than when pretreated with KA2 AS or GluR6 AS alone. Our results suggest that the KA2 subunit is involved in delayed neuronal death induced by cerebral ischemia, at the same time, it is noteworthy that the functional cooperation between KA2 and GluR6 subunits plays a critical role in the ischemic brain injury by PSD95‐MLK3‐MKK4/7‐JNK3 signal pathway. © 2007 Wiley‐Liss, Inc.