OBJECTIVE: This research sought to disclose the regulatory effect of Coriaria lactone (CL) on the Ca(2+)-activated K+ channel in hippocampal pyrimidal neurons of Wistar rats in epileptogenesis. METHODS: Cell-attached and inside-out methods of patch clamp technique were used to record the activity of single channel. The sample data were stored in a computer and analyzed by the application of Pclamp softwares. RESULTS: 1. By means of inside-out method, the KCa channels (120.34 +/- 25.12) pS on the membrane of hippocampal pyrimidal neurons showed a distinct dependence on calcium concentration (n = 6) and on voltage (n = 17), and the channels could be blocked by TEA. 2. With the use of cell-attached method, the KCa channels could be activated by CL apparently (n = 25, P < 0.01). 3. In the conditions where the neuronal membranous voltage was kept at 20 mV and the [Ca2+]i at 10(-8) mol/L in bath solution, the CL at concentrations from 0 microliter/ml to 1.0 microliter/ml could make the open state probability of KCa to increase from 0.025 to 0.553 (P < 0.01), the mean opening time (ms) to prolong from 1.875 +/- 0.412 to 6.829 +/- 0.136, and the mean closing time (ms) to decrease from 179.342 +/- 13.831 to 6.412 +/- 1.383 (n = 25, P < 0.01). CONCLUSION: The membranous KCa activation induced by CL may play an important negative feedback regulating role in the mechanism of epileptogenesis.
OBJECTIVE: This research sought to disclose the regulatory effect of Coriaria lactone (CL) on the Ca(2+)-activated K+ channel in hippocampal pyrimidal neurons of Wistar rats in epileptogenesis. METHODS: Cell-attached and inside-out methods of patch clamp technique were used to record the activity of single channel. The sample data were stored in a computer and analyzed by the application of Pclamp softwares. RESULTS: 1. By means of inside-out method, the KCa channels (120.34 +/- 25.12) pS on the membrane of hippocampal pyrimidal neurons showed a distinct dependence on calcium concentration (n = 6) and on voltage (n = 17), and the channels could be blocked by TEA. 2. With the use of cell-attached method, the KCa channels could be activated by CL apparently (n = 25, P < 0.01). 3. In the conditions where the neuronal membranous voltage was kept at 20 mV and the [Ca2+]i at 10(-8) mol/L in bath solution, the CL at concentrations from 0 microliter/ml to 1.0 microliter/ml could make the open state probability of KCa to increase from 0.025 to 0.553 (P < 0.01), the mean opening time (ms) to prolong from 1.875 +/- 0.412 to 6.829 +/- 0.136, and the mean closing time (ms) to decrease from 179.342 +/- 13.831 to 6.412 +/- 1.383 (n = 25, P < 0.01). CONCLUSION: The membranous KCa activation induced by CL may play an important negative feedback regulating role in the mechanism of epileptogenesis.