Synaptotagmins 1 and 7 in vesicle release from rods of mouse retina.
Synaptotagmins 1 and 7 in vesicle release from rods of mouse retina.
复制标题
DOI：
10.1016/j.exer.2022.109279
复制
发表时间：
2022-12
影响因子：
3.4
通讯作者：
Thoreson, W. B.
中科院分区：
文献类型：
--
作者：
Mesnard, C. S.;Hays, C. L.;Barta, C. L.;Sladek, A. L.;Grassmeyer, J. J.;Hinz, K. K.;Quadros, R. M.;Gurumurthy, C. B.;Thoreson, W. B.
Synaptotagmins are the primary Ca2+ sensors for synaptic exocytosis. Previous work suggested synaptotagmin-1 (Syt1) mediates evoked vesicle release from cone photoreceptor cells in the vertebrate retina whereas release from rods may involve another sensor in addition to Syt1. We found immunohistochemical evidence for syntaptotagmin-7 (Syt7) in mouse rod terminals and so performed electroretinograms (ERG) and single-cell recordings using mice in which Syt1 and/or Syt7 were conditionally removed from rods and/or cones. Synaptic release was measured in mouse rods by recording presynaptic anion currents activated during glutamate re-uptake and from exocytotic membrane capacitance changes. Deleting Syt1 from rods reduced glutamate release evoked by short depolarizing steps but not long steps whereas deleting Syt7 from rods reduced release evoked by long but not short steps. Deleting both sensors completely abolished depolarization-evoked release from rods. Effects of various intracellular Ca2+ buffers showed that Syt1-mediated release from rods involves vesicles close to ribbon-associated Ca2+ channels whereas Syt7-mediated release evoked by longer steps involves more distant release sites. Spontaneous release from rods was unaffected by eliminating Syt7. While whole animal knockout of Syt7 slightly reduced ERG b-waves and oscillatory potentials, selective elimination of Syt7 from rods had no effect on ERGs. Furthermore, eliminating Syt1 from rods and cones abolished ERG b-waves and additional elimination of Syt7 had no further effect. These results show that while Syt7 contributes to slow non-ribbon release from rods, Syt1 is the principal sensor shaping rod and cone inputs to bipolar cells in response to light flashes.
登录
查看更多内容
突触前储存的CA（2+）进入驱动兴奋性的自发神经传递并增强内质网应激。
影响因子：
16.2
作者：
Chanaday NL;Nosyreva E;Shin OH;Zhang H;Aklan I;Atasoy D;Bezprozvanny I;Kavalali ET
通讯作者：
Kavalali ET
DOI：
10.1523/jneurosci.3426-12.2013
发表时间：
2013-01-30
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Chen M;Van Hook MJ;Zenisek D;Thoreson WB
通讯作者：
Thoreson WB
影响因子：
3.4
作者：
Cadetti, Lucia;Bryson, Eric J.;Thoreson, Wallace B.
通讯作者：
Thoreson, Wallace B.
DOI：
10.1085/jgp.202012716
发表时间：
2020-12-07
期刊：
The Journal of general physiology
影响因子：
--
作者：
Hays CL;Sladek AL;Thoreson WB
通讯作者：
Thoreson WB
影响因子：
--
作者：
Harms DW;Quadros RM;Seruggia D;Ohtsuka M;Takahashi G;Montoliu L;Gurumurthy CB
通讯作者：
Gurumurthy CB