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To understand the role of intracellular zinc ion (Zn 2+ ) dysregulation in mediating age-related neurodegenerative changes, particularly neurotoxicity resulting from the generation of excessive neurotoxic amyloid-β (Aβ) peptides, this study aimed to investigate whether N, N, N′, N′-tetrakis (2-pyridylmethyl) ethylenediamine (TPEN), a Zn 2+ -specific chelator, could attenuate Aβ 25–35 -induced neurotoxicity and the underlying electrophysiological mechanism. We used the 3-(4, 5-dimethyl-thiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay to measure the viability of hippocampal neurons and performed single-cell confocal imaging to detect the concentration of Zn 2+  in these neurons. Furthermore, we used the whole-cell patch-clamp technique to detect the evoked repetitive action potential (APs), the voltage-gated sodium and potassium (K + ) channels of primary hippocampal neurons. The analysis showed that TPEN attenuated Aβ 25–35 -induced neuronal death, reversed the Aβ 25–35 -induced increase in intracellular Zn 2+  concentration and the frequency of APs, inhibited the increase in the maximum current density of voltage-activated sodium channel currents induced by Aβ 25–35 , relieved the Aβ 25–35 -induced decrease in the peak amplitude of transient outward K +  currents ( I  A ) and outward-delayed rectifier K +  currents ( I  DR ) at different membrane potentials, and suppressed the steady-state activation and inactivation curves of  I  A  shifted toward the hyperpolarization direction caused by Aβ 25–35 . These results suggest that Aβ 25–35 -induced neuronal damage correlated with Zn 2+  dysregulation mediated the electrophysiological changes in the voltage-gated sodium and K +  channels. Moreover, Zn 2+ -specific chelator-TPEN attenuated Aβ 25–35 -induced neuronal damage by recovering the intracellular Zn 2+  concentration.

molecular brain

TPEN attenuates amyloid-β25–35-induced neuronal damage with changes in the electrophysiological properties of voltage-gated sodium and potassium channels