The effects of rises in external K~+ on the hyperpolarization-activated cation current I_h in rat do

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The effects of rises in external K+(Kext) were examined on the hyperpolarization-activated cation current(Ih) in rat dorsal root ganglion neurons using the whole-cell patch clamp technique.The results showed that Kext increased Ih in a certain concentration and voltage-dependent manner.At the basal Kext level(4 mmol/L),Ih had a maximal amplitude of 1085 ± 340 pA which was enhanced by ~45% and ~92% at 8 and 16 mmol/L Kext,respectively.The midpoint activation voltage was significantly shifted from -98 mV in the hyperpolarizing direction by 8 and 12 mV at 8 and 16 mmol/L Kext,respectively with alteration of the activation course of Ih.The short time constants of activation became longer with the increasing amplitude of the command potential upon rises in Kext.The long time constants became shorter.The reversal potentials were shifted in the positive direction without significant alterations upon rises in Kext.According to the functional role of Ih,Kext increased Ih,resulting in an enhanced neuronal excitability,which might produce activation potential abnormality and perhaps neuropathic pain involved. The effects of rises in external K + (Kext) were examined on the hyperpolarization-activated cation current (Ih) in rat dorsal root ganglion neurons using the whole-cell patch clamp technique. The results showed that Kext increased Ih in a certain concentration and voltage -dependent manner. At the basal Kext level (4 mmol / L), Ih had a maximal amplitude of 1085 ± 340 pA which was enhanced by ~ 45% and ~ 92% at 8 and 16 mmol / L Kext, respectively. activation voltage was significantly shifted from -98 mV in the hyperpolarizing direction by 8 and 12 mV at 8 and 16 mmol / L Kext, respectively with alteration of the activation course of Ih. short time constants of activation longer with the increasing amplitude of the command potential upon rising in Kext. long time constants became shorter. The reversal potentials were shifted in the positive direction without significant alterations upon rises in Kext. According to the functional role of Ih, Kext increased Ih, resulting in an en hanced neuronal excitability, which might produce activation potential abnormality and perhaps neuropathic pain involved.
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