Influences of nanoparticle zinc oxide on acutely isolated rat hippocampal CA3 pyramidal neurons

Abstract

The effects of zinc oxide nanoparticles (nano-ZnO) on the properties of voltage-dependent sodium, potassium currents and evoked action potentials were studied in acutely isolated rat hippocampal CA3 pyramidal neurons at postnatal ages of 10–14 days rats using the whole-cell patch-clamp technique. The results indicated that: (1) in the present of final concentration of 10 −4 g/ml nano-ZnO, the current–voltage curve of sodium current ( I Na) was decreased, and the peak amplitudes of I Na were increased considerably from −50 to +20 mV ( p < 0.05). Meanwhile, the inactivation and the recovery from inactivation of I Na were also promoted by the nano-ZnO solution (10 −4 g/ml) ( p < 0.01). However, the steady-state activation curve of I Na was not shifted by the nano-ZnO. (2) The amplitudes of transient outward potassium current ( I A) were increased by the nano-ZnO solution (10 −4 g/ml), while the current–voltage curve of delayed rectifier potassium current ( I K) was significantly increased from +20 to +90 mV ( p < 0.05). However, it is apparent that the nano-ZnO solution did not shift the steady-state activation curve of I A and I K, and neither had significant effects on the inactivation and the recovery from inactivation of I A. (3) Peak amplitude and overshoot of the evoked single action potential were increased and half-width was diminished in the presence of the 10 −4 g/ml nano-ZnO solution ( p < 0.05). Simultaneously, a prolonged depolarizing current injection enhanced ( p < 0.05) repetitive firing evoked firing rate. These results suggested that 10 −4 g/ml nano-ZnO solution can lead to an enhancement in the current amplitudes of I Na and I K by increasing the opening number of sodium channels, delaying rectifier potassium channels, and enhancing the excitability of neurons, which lead to Na + influx and the accumulation of intracellular Na +, as well as K + efflux plus the loss of cytoplasmic K +. These may disturb the ionic homeostasis and the physiological functions of neurons.