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FEBS Lett. 2008 Apr 16;582(9):1298-306. doi: 10.1016/j.febslet.2008.02.044. Epub 2008 Feb 26.

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

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1
Research Center for Biochemistry and Molecular Biology, Xuzhou Medical College, Xuzhou, Jiangsu 221002, People's Republic of China.

Abstract

In this study, we investigated whether the increase of inhibitory gamma-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.

PMID:
18307989
DOI:
10.1016/j.febslet.2008.02.044
[Indexed for MEDLINE]
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