論文

査読有り
2017年10月

The TRPM1 Channel Is Required for Development of the Rod ON Bipolar Cell-AII Amacrine Cell Pathway in the Retinal Circuit

JOURNAL OF NEUROSCIENCE
  • Takashi Kozuka
  • ,
  • Taro Chaya
  • ,
  • Fuminobu Tamalu
  • ,
  • Mariko Shimada
  • ,
  • Kayo Fujimaki-Aoba
  • ,
  • Ryusuke Kuwahara
  • ,
  • Shu-Ichi Watanabe
  • ,
  • Takahisa Furukawa

37
41
開始ページ
9889
終了ページ
9900
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1523/JNEUROSCI.0824-17.2017
出版者・発行元
SOC NEUROSCIENCE

Neurotransmission plays an essential role in neural circuit formation in the central nervous system (CNS). Although neurotransmission has been recently clarified as a key modulator of retinal circuit development, the roles of individual synaptic transmissions are not yet fully understood. In the current study, we investigated the role of neurotransmission from photoreceptor cells to ON bipolar cells in development using mutant mouse lines of both sexes in which this transmission is abrogated. We found that deletion of the ON bipolar cation channel TRPM1 results in the abnormal contraction of rod bipolar terminals and a decreased number of their synaptic connections with amacrine cells. In contrast, these histological alterations were not caused by a disruption of total glutamate transmission due to loss of the ON bipolar glutamate receptor mGluR6 or the photoreceptor glutamate transporter VGluT1. In addition, TRPM1 deficiency led to the reduction of total dendritic length, branch numbers, and cell body size in AII amacrine cells. Activated Go alpha, known to close the TRPM1 channel, interacted with TRPM1 and induced the contraction of rod bipolar terminals. Furthermore, overexpression of Channelrhodopsin-2 partially rescued rod bipolar cell development in theTRPM1(-/-) retina, whereas the rescue effect by a constitutively closed form of TRPM1 was lower than that by the native form. Our results suggest that TRPM1 channel opening is essential for rod bipolar pathway establishment in development.

Web of Science ® 被引用回数 : 6

リンク情報
DOI
https://doi.org/10.1523/JNEUROSCI.0824-17.2017
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/28899920
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000412800500009&DestApp=WOS_CPL