Oyama Y
Department of Health Sciences, Faculty of Integrated Arts and Sciences, University of Tokushima, Japan.
Brain Res. 1992 Jun 26;583(1-2):93-9. doi: 10.1016/s0006-8993(10)80012-5.
In order to reveal the profile of neurotoxicity of triphenyltin on the mammalian central nervous system (CNS) through the modification of a voltage-dependent Na+ channel, the effects of triphenyltin on the kinetics of voltage-dependent Na+ current (INa) were examined in acutely dissociated pyramidal neurons of rat hippocampus. Triphenyltin at the concentration of 1.10(-6) M decreased both the time to peak and the half-decay time of the INa without affecting the current-voltage relationship. Triphenyltin moved the steady-state inactivation curve to a depolarizing direction. In the presence of triphenyltin, the reactivation of Na+ channel inactivated during the depolarization occurred quicker than that of the control at the pulse intervals of less than 10 ms. It can be suggested that triphenyltin potentially increases the cell excitability in mammalian CNS through the modification of the INa.