Blockade of gap junction hemichannel protects secondary spinal cord injury from activated microglia-mediated glutamate exitoneurotoxicity

We previously demonstrated that activated microglia release excessive glutamate through gap junction hemichannels and identified a novel gap junction hemichannel blocker, INI-0602, that was proven to penetrate the blood-brain barrier and be an effective treatment in mouse models of amyotrophic later...

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Veröffentlicht in:	Journal of neurotrauma 2014-12, Vol.31 (24), p.1967-1974
Hauptverfasser:	Umebayashi, Daisuke, Natsume, Atsushi, Takeuchi, Hideyuki, Hara, Masahito, Nishimura, Yusuke, Fukuyama, Ryuichi, Sumiyoshi, Naoyuki, Wakabayashi, Toshihiko
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Excitatory Amino Acid Antagonists - pharmacology Excitatory Amino Acids - toxicity Female Gap Junctions - drug effects Gap Junctions - metabolism Glutamic Acid - toxicity Heterocyclic Compounds, 4 or More Rings - pharmacology Immunohistochemistry Mice Mice, Inbred C57BL Microglia - metabolism Neurons Neuroprotective Agents - pharmacology Neurotoxicity Neurotransmitters Original Reverse Transcriptase Polymerase Chain Reaction Spinal cord injuries Spinal Cord Injuries - metabolism
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