Effects of SO_(2)derivatives on sodium currents in acutely isolated rat hippocampal lead-exposed neurons

In this study, the effects of acute SO_2 derivatives and chronic lead exposure together on sodium cur-rents (INa) were investigated in acutely isolated rat hippocampal neurons by using the whole-cell patch clamp techniques. We found that chronic lead exposure hardly reduced the amplitudes of INa. In the normal condition, sodium current started to appear at around ?70 mV, and reached the peak current at around ?40 mV. After chronic lead exposure, the data changed to ?70 and ?30 mV. After adding SO2 derivatives, the data changed to ?80 and ?40 mV, respectively. SO_2 derivatives caused a significant in-crease of INa in hippocampal chronic-lead exposed neurons. Chronic lead exposure induced a right shift of the activation curve and a left shift of the inactivation curve of sodium channels. SO_2 derivatives caused negative shifts of the activation and inactivation curves of INa in hippocampal chronic-lead ex-posed neurons. Lead exposure put off the time reaching the peak of INa activation. SO_2 derivatives in-creased the time constants of inactivation after lead exposure. The interaction of lead and SO_2 deriva-tives with voltage-dependent sodium channels may lead to changes in electrical activity and contribute to worsening the neurotoxicological damage.

The effects of rises in external K^+ on the hyperpolarization-activated cation current I_h in rat dorsal root ganglion neurons

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.