OBJECTIVEThe present study was to investigate the effects of acute hypoxia on the electrophysiological properties and outward current of spiral ganglion cell (SGC).

METHODSSGC of newborn's Sprague Dawley (SD) rats were isolated and digested, primary cultured neurons for 8 h. By perfusion with physical saline solution containing no glucose and low oxygen, SGNs model of acute hypoxia was established. The whole-cell patch clamp recording was used to clarify the effect of hypoxia on the outward currents of SGC.

RESULTSThe outward current of SGC showed characteristics of outward rectification, which contained two major components, one sensitive to the big conductance Ca²⁺-activated K⁺ channels (BKCa) which blocked by TEA, and the other could be suppressed by the KV channel blocker 4-AP. When holding at -60 mV, acute hypoxia increased the outward current of SGC in a voltage-dependent manner, which mainly increased the amplitude of the current activated by the votage ranged from 0 mV to +60 mV, and increased the amplitude of outward current from (1 160.0 ± 129.1) pA to (2 428 ± 239.3) pA (n = 9, P < 0.01) at holding potential of -60mV. By perfusion with the Potassium channel blocker TEA or 4-AP, the former could significantly reduced the increasing of outward currents induced by hypoxia on the SGC, the latter had no significant effect on the outward current increased by the hypoxia.

CONCLUSIONSThese results suggest that acute hypoxia causes neuron hyperpolarization possibly by activating big conductance BKCa of the SGC. When the BKca channels are activated, K⁺ effluxes increase, which induces cell membrane hyperpolarization, and decreases cell excitability, which may affect the conducting function of SGC.