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A novel mechanism of zinc block on α1G-like low-threshold T-type Ca2+ channels in a rat thalamic relay neuron
- A novel mechanism of zinc block on α1G-like low-threshold T-type Ca2+ channels in a rat thalamic relay neuron
- Noh J.; Kim M.-k.; Chung J.-m.
- Ewha Authors
- SCOPUS Author ID
- Issue Date
- Journal Title
- Neuroscience Research
- vol. 66, no. 4, pp. 353 - 358
- SCI; SCIE; SCOPUS
- To elucidate biophysical mechanisms underlying the Zn2+ block on the low-threshold T-type Ca2+ current (IT), we examined the Zn2+-induced alterations of gating properties of IT of a rat thalamic relay neuron and of α1G channels expressed in HEK-293 cells, using a whole-cell voltage clamp technique. The effect of Zn2+ block depended upon holding potentials but not test potentials, indicating that, the greater the inactivation, the less Zn2+ blocked IT. Except for the inactivation near the activation threshold of IT, no significant changes in the kinetics of activation and inactivation were induced by Zn2+. In contrast, the rates of both de-inactivation and deactivation were dramatically increased by Zn2+, and moreover the channels were rapidly re-blocked upon re-polarization under Zn2+. Furthermore, the outward current via α1G channel was almost insensitive to Zn2+. All these results imply that Zn2+ alters the gating properties of IT mainly by accelerating its deactivation process. © 2009 Elsevier Ireland Ltd and the Japan Neuroscience Society.
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