| Autor: |
Takashi Kozuka, Taro Chaya, Fuminobu Tamalu, Mariko Shimada, Kayo Fujimaki-Aoba, Ryusuke Kuwahara, Shu-Ichi Watanabe, Takahisa Furukawa |
| Předmět: |
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| Zdroj: |
Journal of Neuroscience; 10/11/2017, Vol. 37 Issue 41, p9889-9900, 12p |
| Abstrakt: |
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 VGluT 1. In addition, TRPM1 deficiency led to the reduction of total dendritic length, branch numbers, and cell body size in All amacrine cells. Activated Goa, 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 the TRPM -/-retina, whereas the rescue effect by a constitutively closed form of TRPM 1 was lower than that by the native form. Our results suggest that TRPM 1 channel opening is essential for rod bipolar pathway establishment in development. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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