Effects of acute hypoxia on potassium channels in spiral ganglion cells of SD rats
10.3760/cma.j.issn.1673-0860.2015.10.007
- VernacularTitle:急性缺氧对SD乳鼠耳蜗螺旋神经节细胞钾通道的影响
- Author:
Yanping WANG
1
;
He ZHU
;
Ketao MA
;
Junqiang SI
;
Li LI
Author Information
1. 石河子大学医学院生理教研室新疆地方与民族高发病教育部重点实验室
- Keywords:
Spiral ganglion;
Cell hypoxia;
Large-conductance calcium-activated potassium channels;
Potassium channels,voltage-gated;
Patch-clamp techniques;
Rats,Sprague-Dawley
- From:
Chinese Journal of Otorhinolaryngology Head and Neck Surgery
2015;50(10):823-828
- CountryChina
- Language:Chinese
-
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 voltagedependent 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.
