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Neuroprotection of Ischemic Postconditioning by
Downregulating the Postsynaptic Signaling Mediated by
Kainate Receptors
by Jing Liu, Qin Xu, Hui Wang, Ran Wang, and Xiao-Yu Hou
Stroke
Volume 44(7):2031-2035
June 24, 2013
Copyright © American Heart Association, Inc. All rights reserved.
Phosphoinositide 3-kinase (PI3K) pathway, but not mitogen-activated protein kinase kinase 1
(MEK1) pathway, associates with the neuroprotection of the postconditioning against global
ischemia in the rat hippocampal CA1 subregion.
Jing Liu et al. Stroke. 2013;44:2031-2035
Copyright © American Heart Association, Inc. All rights reserved.
Phosphoinositide 3-kinase (PI3K) pathway, but not mitogen-activated protein kinase kinase 1
(MEK1) pathway, is involved in the postconditioning-induced inhibition of both glutamatergic
kainate receptor subunit 2 (GluK2)–postsynaptic density protein-95 (PSD-95)–mixed lineage
kinase 3 (MLK3) assembly and MLK3–mitogen-activated protein kinase kinase 7 (MKK7)–c-Jun
N-terminal kinase 3 (JNK3) signaling.
Jing Liu et al. Stroke. 2013;44:2031-2035
Copyright © American Heart Association, Inc. All rights reserved.
Akt pathway is responsible for the postconditioning-induced neuroprotection and
downregulation of glutamatergic kainate receptor subunit 2 (GluK2)–postsynaptic density
protein-95 (PSD-95)–mixed lineage kinase 3 (MLK3)–c-Jun N-terminal kinase 3 (JNK3) signaling.
Jing Liu et al. Stroke. 2013;44:2031-2035
Copyright © American Heart Association, Inc. All rights reserved.
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