期刊
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
卷 30, 期 6, 页码 1247-1260出版社
SAGE PUBLICATIONS INC
DOI: 10.1038/jcbfm.2010.30
关键词
acid-sensing ion channel; brain injury; human; neuron; patch clamp
资金
- National Institute of Health [R01NS47506, R01NS50610]
- American Heart Association [0840132N]
- Legacy Research Advisory Committee
Acidosis is a common feature of the human brain during ischemic stroke and is known to cause neuronal injury. However, the mechanism underlying acidosis-mediated injury of the human brain remains elusive. We show that a decrease in the extracellular pH evoked inward currents characteristic of acid-sensing ion channels (ASICs) and increased intracellular Ca2+ in cultured human cortical neurons. Acid-sensing ion channels in human cortical neurons show electrophysiological and pharmacological properties distinct from those in neurons of the rodent brain. Reverse transcriptase-PCR and western blot detected a high level of the ASIC1a subunit with little or no expression of other ASIC subunits. Treatment of human cortical neurons with acidic solution induced substantial cell injury, which was attenuated by the ASIC1a blockade. Thus, functional homomeric ASIC1a channels are predominantly expressed in neurons from the human brain. Activation of these channels has an important role in acidosis-mediated injury of human brain neurons. Journal of Cerebral Blood Flow & Metabolism (2010) 30, 1247-1260; doi: 10.1038/jcbfm.2010.30; published online 10 March 2010
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