Abstract

The effect of Radix paeoniae rubra (RPR) on voltage-gated sodium channel (VGSC) currents ( I Na) was examined in freshly isolated rat hippocampal CA1 neurons using whole-cell patch-clamp technique under voltage-clamp conditions. RPR suppressed I Na without affecting the current activation, inactivation and deactivation. The amplitude of I Na decreased by ∼18.4% within a few seconds of 0.8 mg/ml RPR exposure. RPR (0.8 mg/ml) shifted the steady-state inactivation curves of I Na to negative potentials, with hyperpolarizing direction shift of V 1/2 of 10.0 mV. The time course of I Na recovery from inactivation was prolonged significantly by 0.8 mg/ml RPR. RPR (0.8 mg/ml) also enhanced the activity-dependent attenuation of I Na and decreased the fraction of activated channels. These results suggested that RPR suppressed hippocampal CA1 I Na by shifting the inactivation curve in hyperpolarizing direction, slowing the recovery time course from inactivation, enhancing the activity-dependent attenuation and decreasing the number of activatable channels. RPR suppression on I Na might predict the protective effect during brain ischemia in hippocampal CA1 neurons.

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