Neuroprotection of ethanol against ischemia/reperfusion-induced brain injury through decreasing c-Jun N-terminal kinase 3 (JNK3) activation by enhancing GABA release

Abstract Our latest study indicated that ethanol could attenuate cerebral ischemia/reperfusion-induced brain injury through activating Ionotropic glutamate receptors Kainate Family (Gluk1)–kainate (KA) receptors and gamma-aminobutyric acid (GABA) receptors. However, the possible mechanism of the neu...

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Veröffentlicht in:	Neuroscience 2010-06, Vol.167 (4), p.1125-1137
Hauptverfasser:	Qi, S.-H, Liu, Y, Hao, L.-Y, Guan, Q.-H, Gu, Y.-H, Zhang, J, Yan, H, Wang, M, Zhang, G.-Y
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Apoptosis Apoptosis - drug effects Bicuculline - pharmacology Biological and medical sciences Brain Ischemia - metabolism Brain Ischemia - pathology Brain Ischemia - prevention & control brain ischemia-reperfusion c-Jun N-terminal kinase 3 (JNK3) CA1 Region, Hippocampal - drug effects CA1 Region, Hippocampal - metabolism CA1 Region, Hippocampal - pathology Cadmium Chloride - pharmacology Calcium Channel Blockers - pharmacology Enzyme Activation ethanol Ethanol - pharmacology Ethanol - therapeutic use Fundamental and applied biological sciences. Psychology GABA GABA-A Receptor Antagonists gamma-Aminobutyric Acid - metabolism In Vitro Techniques Inhibitory Postsynaptic Potentials - drug effects Male Medical sciences Miniature Postsynaptic Potentials - drug effects Mitogen-Activated Protein Kinase 10 - metabolism Neurology Neurons - drug effects Neurons - pathology neuroprotection Neuroprotective Agents - pharmacology Neuroprotective Agents - therapeutic use Patch-Clamp Techniques Phosphorylation Rats Rats, Sprague-Dawley Reperfusion Injury - metabolism Reperfusion Injury - pathology Reperfusion Injury - prevention & control Vascular diseases and vascular malformations of the nervous system Vertebrates: nervous system and sense organs
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