BK channels modulate pre- and postsynaptic signaling at reciprocal synapses in retina.
BK channels modulate pre- and postsynaptic signaling at reciprocal synapses in retina.
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DOI：
10.1038/nn.2302
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发表时间：
2009-05
影响因子：
25
通讯作者：
Diamond, Jeffrey S.
中科院分区：
文献类型：
--
作者：
Grimes, William N.;Li, Wei;Chavez, Andres E.;Diamond, Jeffrey S.
在哺乳动物视网膜中，A17无突细胞向杆双极细胞提供相互抑制反馈，从而形成体内视觉信号的时间过程。先前的研究结果表明，A17反馈可以通过Ca2+可渗透的ampar被Ca2+内流触发，并且可以独立于电压门控Ca2+ (Cav)通道发生，其在A17树突中的存在和功能作用尚未被探索。在这里，我们结合电生理学、钙成像和免疫组织化学表明，大鼠A17腺分泌细胞中的l型Cav通道位于突触互反馈的位置，但它们对GABA释放的贡献被大电导Ca2+活化钾（BK）通道所削弱，后者抑制了A17突触后去极化并限制了Cav通道的激活。我们还发现BK通道通过限制A17s释放GABA来调节通过杆通路的兴奋性突触传递。
In the mammalian retina, A17 amacrine cells provide reciprocal inhibitory feedback to rod bipolar cells, thereby shaping the time course of visual signaling in vivo. Previous results indicate that A17 feedback can be triggered by Ca2+ influx through Ca2+ permeable AMPARs and can occur independently of voltage-gated Ca2+ (Cav) channels, whose presence and functional role in A17 dendrites have not been explored. Here, we combine electrophysiology, calcium imaging and immunohistochemistry to show that L-type Cav channels in rat A17 amacrine cells are located at the sites of reciprocal synaptic feedback, but their contribution to GABA release is diminished by large-conductance Ca2+-activated potassium (BK) channels, which suppress postsynaptic depolarization in A17s and limit Cav channel activation. We also show that BK channels, by limiting GABA release from A17s, regulate the flow of excitatory synaptic transmission through the rod pathway.
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DOI：
10.1152/nips.01387.2002
发表时间：
2002-08-01
期刊：
NEWS IN PHYSIOLOGICAL SCIENCES
影响因子：
--
作者：
Orio, P;Rojas, P;Latorre, R
通讯作者：
Latorre, R
影响因子：
2.5
作者：
Hartveit, E
通讯作者：
Hartveit, E
影响因子：
5.3
作者：
Hu, H;Shao, LR;Storm, JF
通讯作者：
Storm, JF
DOI：
10.1073/pnas.96.7.4137
发表时间：
1999-03-30
影响因子：
11.1
作者：
Wallner, M;Meera, P;Toro, L
通讯作者：
Toro, L
影响因子：
2.5
作者：
NELSON, R;KOLB, H
通讯作者：
KOLB, H