Blockade of Gap Junction Hemichannel Protects Secondary Spinal Cord Injury from Activated Microglia-Mediated Glutamate Exitoneurotoxicity-Reference-Cited by-同舟云学术

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Blockade of Gap Junction Hemichannel Protects Secondary Spinal Cord Injury from Activated Microglia-Mediated Glutamate Exitoneurotoxicity

Published:2014-12-15 Issue:24 Volume:31 Page:1967-1974
ISSN:0897-7151
Container-title:Journal of Neurotrauma
language:en
Short-container-title:Journal of Neurotrauma

Author:

Umebayashi Daisuke¹,Natsume Atsushi¹,Takeuchi Hideyuki²,Hara Masahito¹,Nishimura Yusuke¹,Fukuyama Ryuichi,Sumiyoshi Naoyuki³,Wakabayashi Toshihiko¹

Affiliation:

1. Department of Neurosurgery, Nagoya University School of Medicine, Nagoya, Japan.

2. Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan.

3. Division of Pathology, Konan Kosei Hospital, Aichi, Japan.

Publisher

Mary Ann Liebert Inc

Subject

Neurology (clinical)

Link

http://www.liebertpub.com/doi/pdf/10.1089/neu.2013.3223

Reference41 articles.

1. Neurotoxicity by microglia: Mechanisms and potential therapeutic strategy

2. Ischemic Damage in Hippocampal CA1 is Dependent on Glutamate Release and Intact Innervation from CA3

3. Glutamate neurotoxicity in cortical cell culture is calcium dependent

4. Tumor Necrosis Factor-α Induces Neurotoxicity via Glutamate Release from Hemichannels of Activated Microglia in an Autocrine Manner

5. Activation of microglia by secreted amyloid precursor protein evokes release of glutamate by cystine exchange and attenuates synaptic function

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