The neurotoxic effects of N-methyl-N-nitrosourea on the electrophysiological property and visual signal transmission of rat's retina.
The neurotoxic effects of N-methyl-N-nitrosourea on the electrophysiological property and visual signal transmission of rat's retina.
复制标题
N-甲基-N-亚硝基脲对大鼠视网膜电生理特性和视觉信号传递的神经毒性作用。
DOI：
10.1016/j.taap.2015.03.013
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发表时间：
2015-07
期刊：
影响因子：
--
通讯作者：
刘备
中科院分区：
文献类型：
--
作者：
刘备
The neurotoxic effects of N-methyl-N-nitrosourea (MNU) on the inner retinal neurons and related visual signal circuits have not been described in any animal models or human, despite ample morphological evidences about the MNU induced photoreceptor (PR) degeneration. With the helping of MEA (multielectrode array) recording system, we gained the opportunity to systemically explore the neural activities and visual signal pathways of MNU administrated rats. Our MEA research identified remarkable alterations in the electrophysiological properties and firstly provided instructive information about the neurotoxicity of MNU that affects the signal transmission in the inner retina. Moreover, the spatial electrophysiological functions of retina were monitored and found that the focal PRs had different vulnerabilities to the MNU. The MNU-induced PR dysfunction exhibited a distinct spatial- and time-dependent progression. In contrast, the spiking activities of both central and peripheral RGCs altered synchronously in response to the MNU administration. Pharmacological tests suggested that gap junctions played a pivotal role in this homogeneous response of RGCs. SNR analysis of MNU treated retina suggested that the signaling efficiency and fidelity of inner retinal circuits have been ruined by this toxicant, although the microstructure of the inner retina seemed relatively consolidated. The present study provided an appropriate example of MEA investigations on the toxicant induced pathological models and the effects of the pharmacological compounds on neuron activities. The positional MEA information would enrich our knowledge about the pathology of MNU induced RP models, and eventually be instrumental for elucidating the underlying mechanism of human RP.
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影响因子：
1.1
作者：
Jeong E;Paik SS;Jung SW;Chun MH;Kim IB
通讯作者：
Kim IB
影响因子：
3.8
作者：
E. Lee;C. Garner;T. Terzo
通讯作者：
E. Lee;C. Garner;T. Terzo
影响因子：
2.2
作者：
K. Yoshizawa;Maki Kuwata;Ayako Kawanaka;N. Uehara;T. Yuri;A. Tsubura
通讯作者：
K. Yoshizawa;Maki Kuwata;Ayako Kawanaka;N. Uehara;T. Yuri;A. Tsubura
影响因子：
3.4
作者：
M. Mela;S. R. Grötzner;A. Legeay;N. Mesmer-Dudons;J. Massabuau;D. Ventura;C. A. de Oliveira Ribeiro
通讯作者：
M. Mela;S. R. Grötzner;A. Legeay;N. Mesmer-Dudons;J. Massabuau;D. Ventura;C. A. de Oliveira Ribeiro
DOI：
10.1097/00006982-200004000-00010
发表时间：
2000-04
期刊：
Retina
影响因子：
--
作者：
Apichart Singalavanija;N. Ruangvaravate;D. Dulayajinda
通讯作者：
Apichart Singalavanija;N. Ruangvaravate;D. Dulayajinda