Various voltage-gated K+ currents were recently described in dorsal root ganglion (DRG) neurons. However, the characterization and diversity of voltage-gated K+ currents have not been well studied in trigeminal root ganglion (TRG) neurons, which are similar to the DRG neurons in terms of physiological roles and anatomy. This study was aimed to investigate the characteristics and diversity of voltage-gated K+ currents in acutely isolated TRG neurons of rat using whole cell patch clamp techniques. The first type (type I) had a rapid, transient outward current (IA) with the largest current size having a slow inactivation rate and a sustained delayed rectifier outward current (IK) that was small in size having a fast inactivation rate. The IA currents of this type were mostly blocked by TEA and 4-AP, K channel blockers whereas the IK current was inhibited by TEA but not by 4-AP. The second type had a large IA current with a slow inactivation rate and a medium size-sustained delayed IK current with a slow inactivation rate. In this second type (type II), the sensitivities of the IA or IK current by TEA and 4-AP were similar to those of the type I. The third type (type III) had a medium sized IA current with a fast inactivation rate and a large sustained IK current with the slow inactivation rate. In type III current, TEA decreased both IA and IK but 4-AP only blocked IA current. The fourth type (type IV) had a smallest IA with a fast inactivation rate and a large IK current with a slow inactivation rate. TEA or 4-AP similarly decreased the IA but the IK was only blocked by 4-AP. These findings suggest that at least four different voltage-gated K+ currents in biophysical and pharmacological properties exist in the TRG neurons of rats.

Cyclosporin A (CsA) plays an important role in clinical medicine and basic biology as an immunosuppressant and a mitochondrial permeability blocker, respectively. It was reported that CsA has a protective role by preventing apoptosis and promoting the proliferation in severed neurons. However, the molecular mechanisms for CsA-induced neuronal cell proliferation are unclear. In this study, we examined the mechanisms underlying the CsA-induced proliferation of PC12 cells. CsA increased the viability of PC12 cells in a dose(over 0.1~10 μM)-and time-dependent manner. The level of ROS generation was decreased in the CsA-treated PC12 cells. Expression of Bcl-2, an antiapoptotic molecule that inhibits the release of cytochrome c from the mitochondria into the cytosol, was upregulated, whereas Bax, a proapototic molecule, was not changed in the CsA-treated PC12 cells. CsA downregulated the mRNA expression of VDAC 1 and VDAC 3, but VDAC 2 was not changed in the CsA-treated PC12 cells. The level of cytosolic cytochrome c released from the mitochondria and the caspase-3 activity were attenuated in the CsA-treated PC12 cells. These results suggest that the mitochondria-mediated apoptotic signal and Bcl-2 family may play an important role in CsA-induced proliferation in PC12 cells.