Waldmann R
Institut de Pharmacologie Moléculaire et Cellulaire-CNRS, Sophia-Antipolis, Valbonne, France.
Adv Exp Med Biol. 2001;502:293-304. doi: 10.1007/978-1-4757-3401-0_19.
Metabolic hyperactivity or limited oxygen supply can cause a decrease of tissue pH. Severe tissue acidosis that accompanies ischemia and most forms of inflammation is painful and sensory neurons respond to acidic tissue pH with increased firing. H+-gated cation channels in sensory nerve endings are thought to be responsible for the activation of nociceptive afferents by acid. The members of one family of recently identified H+-gated cation channels (ASICs, Acid Sensing Ion Channels) are candidates for the acid sensor in sensory nerve endings. Certain ASIC subunits are also or exclusively expressed in neurons of the central nervous system (CNS) where the role of those cation channels is as for yet unknown. Neuronal activity is accompanied by pH fluctuations and the widespread expression of ASIC channels throughout the CNS suggests that activation of those ion channels by local acidic transients might play a role in neurotransmission or neuromodulation.
代谢亢进或氧气供应受限可导致组织pH值降低。伴随局部缺血和大多数炎症形式出现的严重组织酸中毒是疼痛的，感觉神经元会对酸性组织pH值做出反应，放电增加。感觉神经末梢中的H⁺门控阳离子通道被认为是酸激活伤害性传入神经的原因。最近发现的一个H⁺门控阳离子通道家族（ASICs，酸敏感离子通道）的成员是感觉神经末梢酸传感器的候选者。某些ASIC亚基也在或仅在中枢神经系统（CNS）的神经元中表达，这些阳离子通道在其中的作用尚不清楚。神经元活动伴随着pH值波动，ASIC通道在整个中枢神经系统中的广泛表达表明，局部酸性瞬变对这些离子通道的激活可能在神经传递或神经调节中起作用。
