Abstract
Nitric oxide (NO) is a diffusible second messenger, which regulates neurotransmission, serving as the principal endothelium-derived relaxing factor. NO also acts as an ion channel modulator. Nitric oxide synthase (NOS) has been identified in the inner ear, although its physiological role remains unclear. In the present study, the effects of NO onto K currents in inner hair cells (IHCs) were investigated. IHCs were acutely isolated and K currents were recorded by conventional whole-cell voltage-clamp recordings. NO donors sodium nitroprusside (SNP) were applied directly to the cells. In 1mM SNP solutions, the amplitude of outward K currents (IK,f and IK,s) reversely decreased; however, fast activation kinetics was preserved. In the current-voltage relationship curves, the maximal slope conductances were 53.2nS and 44.2nS in control solutions and 1mM SNP solutions, respectively. At the membrane potential of +110mV, the amplitudes of outward currents were 9.2±2.9nA in control solutions and 7.3±2.7nA in 1mM SNP solutions, showing a significant difference. NO acts as a K channel modulator in IHCs. A fast K current suppression may account for the high-frequency hearing impairment by the prevention of fast repolarization.
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