Nano-CuO inhibited voltage-gated sodium current of hippocampal CA1 neurons via reactive oxygen species but independent from G-proteins pathway

Z. Liu; S. Liu; Guogang Ren; T. Zhang; Z. Yang

doi:10.1002/jat.1611

Nano-CuO inhibited voltage-gated sodium current of hippocampal CA1 neurons via reactive oxygen species but independent from G-proteins pathway

Z. Liu, S. Liu, Guogang Ren, T. Zhang, Z. Yang

Research output: Contribution to journal › Article › peer-review

41 Citations (Scopus)

Abstract

The aim of this study was to investigate the effects of nano-CuO on voltage-gated sodium current (INa) in hippocampal CA1 neurons. The results suggested that nano-CuO inhibited amplitudes of INa currents and prolonged peak rise time of action potential (AP). The responses to nano-CuO were inhibited by reactive oxygen species (ROS) scavenger. However, the G-proteins inhibitor did not block the effects of nano-CuO. The effects of nano-CuO were mediated through activation of ROS-INa-AP signaling cascades and independent from G-proteins pathway.

Original language	English
Pages (from-to)	439-445
Journal	Journal of Applied Toxicology
Volume	31
Issue number	5
DOIs	https://doi.org/10.1002/jat.1611
Publication status	Published - 2011

Keywords

hippocampus
nano-CuO
reactive oxygen species
voltage-gated sodium current

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10.1002/jat.1611

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title = "Nano-CuO inhibited voltage-gated sodium current of hippocampal CA1 neurons via reactive oxygen species but independent from G-proteins pathway",

abstract = "The aim of this study was to investigate the effects of nano-CuO on voltage-gated sodium current (INa) in hippocampal CA1 neurons. The results suggested that nano-CuO inhibited amplitudes of INa currents and prolonged peak rise time of action potential (AP). The responses to nano-CuO were inhibited by reactive oxygen species (ROS) scavenger. However, the G-proteins inhibitor did not block the effects of nano-CuO. The effects of nano-CuO were mediated through activation of ROS-INa-AP signaling cascades and independent from G-proteins pathway.",

keywords = "hippocampus, nano-CuO, reactive oxygen species, voltage-gated sodium current",

author = "Z. Liu and S. Liu and Guogang Ren and T. Zhang and Z. Yang",

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T1 - Nano-CuO inhibited voltage-gated sodium current of hippocampal CA1 neurons via reactive oxygen species but independent from G-proteins pathway

AU - Liu, Z.

AU - Liu, S.

AU - Ren, Guogang

AU - Zhang, T.

AU - Yang, Z.

N1 - The definitive version can be found at: http://onlinelibrary.wiley.com/ Copyright Wiley-Blackwell [Full text of this article is not available in the UHRA]

PY - 2011

Y1 - 2011

N2 - The aim of this study was to investigate the effects of nano-CuO on voltage-gated sodium current (INa) in hippocampal CA1 neurons. The results suggested that nano-CuO inhibited amplitudes of INa currents and prolonged peak rise time of action potential (AP). The responses to nano-CuO were inhibited by reactive oxygen species (ROS) scavenger. However, the G-proteins inhibitor did not block the effects of nano-CuO. The effects of nano-CuO were mediated through activation of ROS-INa-AP signaling cascades and independent from G-proteins pathway.

AB - The aim of this study was to investigate the effects of nano-CuO on voltage-gated sodium current (INa) in hippocampal CA1 neurons. The results suggested that nano-CuO inhibited amplitudes of INa currents and prolonged peak rise time of action potential (AP). The responses to nano-CuO were inhibited by reactive oxygen species (ROS) scavenger. However, the G-proteins inhibitor did not block the effects of nano-CuO. The effects of nano-CuO were mediated through activation of ROS-INa-AP signaling cascades and independent from G-proteins pathway.

KW - hippocampus

KW - nano-CuO

KW - reactive oxygen species

KW - voltage-gated sodium current

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M3 - Article

SN - 0260-437X

VL - 31

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EP - 445

JO - Journal of Applied Toxicology

JF - Journal of Applied Toxicology

IS - 5

ER -

Nano-CuO inhibited voltage-gated sodium current of hippocampal CA1 neurons via reactive oxygen species but independent from G-proteins pathway

Abstract

Keywords

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