title: [Effects of acute hypoxia on potassium channels in spiral ganglion cells of SD rats].
abstract: OBJECTIVE
  The present study was to investigate the effects of acute hypoxia on the electrophysiological properties and outward current of spiral ganglion cell (SGC).
  
  
  METHODS
  SGC 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.
  
  
  RESULTS
  The 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.
  
  
  CONCLUSIONS
  These 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.
authors.affiliation: Department of Physiology, Shihezi University Medical College and the Key Laboratory of Xinjiang Endemic and Ethnic Diseases, Shihezi 832002, China.
authors.forename: Yanping
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Physiology, Shihezi University Medical College and the Key Laboratory of Xinjiang Endemic and Ethnic Diseases, Shihezi 832002, China.
authors.forename: He
authors.initials: H
authors.lastname: Zhu
authors.affiliation: Department of Physiology, Shihezi University Medical College and the Key Laboratory of Xinjiang Endemic and Ethnic Diseases, Shihezi 832002, China.
authors.forename: Ketao
authors.initials: K
authors.lastname: Ma
authors.affiliation: Department of Physiology, Shihezi University Medical College and the Key Laboratory of Xinjiang Endemic and Ethnic Diseases, Shihezi 832002, China.
authors.forename: Junqiang
authors.initials: J
authors.lastname: Si
authors.affiliation: Department of Physiology, Shihezi University Medical College and the Key Laboratory of Xinjiang Endemic and Ethnic Diseases, Shihezi 832002, China; Email: lily7588@163.com.
authors.forename: Li
authors.initials: L
authors.lastname: Li
mesh_terms: D000818:Animals; D000860:Hypoxia / Q000503:physiopathology*; D009474:Neurons / Q000166:cytology / Q000378:metabolism*; D018408:Patch-Clamp Techniques; D015221:Potassium Channels / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013136:Spiral Ganglion / Q000166:cytology / Q000503:physiopathology*
chemical_list: D015221:Potassium Channels