Zinc ion as modulator effects on excitability and synaptic transmission in hippocampal CA1 neurons in Wistar rats.

Zinc is one of trace elements that play essential roles in several cell functions, and is unquestionably important to the normal health and function of the central nervous system. Growing evidence suggests that Zn(2+) can become a pathogenic agent in certain neurological disease states, such as ischemia, seizures, and trauma. The main role of the Zn(2+) may serve as an endogenous neuromodulator in the brain. In the present study, we used the electrophysiology method to investigate the effects of Zn(2+) on the excitability of hippocampus CA1 region. Our results have demonstrated that the Zn(2+) activates the Wistar rat hippocampal CA1 region network by significantly enhancing the spike rate of the spontaneous firing. In addition, Zn(2+) can increase the intrinsic membrane excitability by enhancing the firing rate and half-width of the evoked action potential. Meanwhile, our results also indicate that Zn(2+) can effectively inhibit voltage-dependent potassium currents (both transient outward potassium currents and delayed rectifier potassium currents). On the other hand, Zn(2+) also inhibits excitatory neurotransmitter release by decreasing the inter-event interval and the total charge transfer of the excitatory postsynaptic currents. The present results, in combination with other works, suggest that Zn(2+) can influence neuronal excitability, intrinsic membrane excitability and synaptic transmission in the hippocampus CA1 neurons by multiple mechanisms.