作者: Rainer Waldmann
DOI: 10.1007/978-1-4757-3401-0_19
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摘要: Metabolic hyperactivity or limited oxygen supply can cause a decrease of tissue pH. Severe acidosis that accompanies ischemia and most forms inflammation is painful sensory neurons respond to acidic pH with increased firing. H+-gated cation channels in nerve endings are thought be responsible for the activation nociceptive afferents by acid. The members one family recently identified (ASICs, Acid Sensing Ion Channels) candidates acid sensor endings. Certain ASIC subunits also exclusively expressed central nervous system (CNS) where role those as yet unknown. Neuronal activity accompanied fluctuations widespread expression throughout CNS suggests ion local transients might play neurotransmission neuromodulation.