ABSTRACT
AIM: To investigate the effects of rat retinal ganglion cell (RGC) apoptosis on delayed rectifier K+currents (IK).METHODS:The retinas of 2~3 d newborn Sprague-Dawley rats were dissociated into cell suspension by trypsin digestion .The RGCs were cultured and divided into control group , pressure 0.5 h group, pressure 1 h group, pressure 1.5 h group and pressure 2 h group.The cells were cultured regularly for 6 d in control group , and the cells in other groups were cultured regularly for 6 d and gave pressure of 80 mmHg for 0.5 h, 1 h, 1.5 h and 2 h, respectively. The rhodamine 123 fluorescence from labeled RGC mitochondrion was detected by continuous wavelength multifunctional microplate detection instrument.The membrane capacitance (Cm) in different groups and IK in the pressure 1 h group were recorded from the RGCs by whole-cell patch-clamp technique .RESULTS:No difference of rhodamine 123 fluorescence in the RGC mitochondria between control group and pressure 0.5 h group was observed .Rhodamine 123 fluorescence in the other 3 groups was significantly lower than that in control group (P<0.05).No difference of the Cm between control group and pressure 0.5 h group was found, and the Cm in the other 3 groups was significantly lower than that in control group (P<0.05).The amplitudes of IK were higher than that in control group .At the test potential from -10 mV to 60 mV, the current density in pressure 1 h group was significantly higher than that in control group (P<0.05).The maximal conduc-tion ( Gmax ) in pressure 1 h group was significantly higher than that in control group .The voltage for IK channel half-activa-tion ( V1/2 ) in pressure 1 h group declined comparison with control group ( P<0.01 ) , and the k value had no significant difference between the 2 groups.CONCLUSION:Retinal ganglion cell apoptosis accompanies with delayed rectifier K +current enhancement .
ABSTRACT
BACKGROUND: Propofol (2,6-diisopropylphenol) is a widely used intravenous anesthetic, and the effects of propofol on several ion channels have been studied at the whole cell and single-channel levels. However, in general there is no report on the effect of propofol on outward K+ currents in canine colonic myocytes, in which there are two types of outward K+ currents, a large-conductance Ca2+-activated K+ current and a classical delayed rectifier K+ current. We examined the effects of propofol on the two types of outward K+ currents the kinetics involved. METHODS: Experiments were performed on freshly dispersed smooth muscle cells from the circular muscle layer of the proximal canine colon. Outward currents were recorded using the patch clamp technique in the whole cell configuration. RESULTS: The application of propofol (600 nM-600microM) decreased net outward current in a dose-dependent manner. Propofol (6-60microM) also decreased peak delayed rectifier K+ currents. Pretreatment with TEA abolished propofol effects on delayed rectifier K+ currents. However, propofol still decreased delayed rectifier K+ currents in the presence of 4-AP. CONCLUSIONS: These data suggest that propofol decrease net outward K+ currents primarily by inhibiting large-conductance Ca2+-activated K+ currents and 4-AP resistant delayed rectifier K+ currents. These results suggest that propofol action on outward currents may depend on the different blocking mechanisms of the different types of K+ channels. If propofol cannot induce contraction, Ca2+ currents in colonic myocytes warrant further study.