Co-activation of GABA receptors inhibits the JNK3 apoptotic pathway via the disassembly of the GluR6-PSD95-MLK3 signaling module in cerebral ischemic-reperfusion

Dong Han, Quanguang Zhang, Yong-Liu, Chong Li, Yan Yan Zong, Chang Zhou Yu, Wei Wang, Jing Zhi Yan, Guang Yi Zhang

Research output: Contribution to journalArticle

20 Scopus citations


In this study, we investigated whether the increase of inhibitory γ-amino butyric acid (GABA) signal suppresses the excitatory glutamate signal induced by cerebral ischemia and the underlying mechanisms. In global cerebral ischemia, focal cerebral ischemia and oxygen-glucose deprivation, application of muscimol and baclofen, agonists of GABA(A) receptor and GABA(B) receptor, exerted neuroprotection. The agonists inhibited the increased assembly of the GluR6-PSD-95-MLK3 module induced by cerebral ischemia and the activation of the MLK3-MKK4/7-JNK3 cascade. Our results suggest that stimulation of the inhibitory GABA receptors can attenuate the excitatory JNK3 apoptotic signaling pathway via inhibiting the increased assembly of the GluR6-PSD-95-MLK3 signaling module in cerebral ischemia.

Original languageEnglish (US)
Pages (from-to)1298-1306
Number of pages9
JournalFEBS Letters
Issue number9
Publication statusPublished - Apr 16 2008



  • Baclofen
  • Cerebral ischemia
  • JNK pathway
  • Muscimol
  • Neuroprotection

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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