University of Hertfordshire

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

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Original languageEnglish
Pages (from-to)220-230
Publication statusPublished - 2009


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 (INa) was decreased, and the peak amplitudes of INa were increased considerably from −50 to +20 mV (p < 0.05). Meanwhile, the inactivation and the recovery from inactivation of INa were also promoted by the nano-ZnO solution (10−4 g/ml) (p < 0.01). However, the steady-state activation curve of INa was not shifted by the nano-ZnO. (2) The amplitudes of transient outward potassium current (IA) were increased by the nano-ZnO solution (10−4 g/ml), while the current–voltage curve of delayed rectifier potassium current (IK) 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 IA and IK, and neither had significant effects on the inactivation and the recovery from inactivation of IA. (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 INa and IK 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.


Original article can be found at : Copyright Elsevier

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