Ih channels control feedback regulation from amacrine cells to photoreceptors.
Ih channels control feedback regulation from amacrine cells to photoreceptors.
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DOI：
10.1371/journal.pbio.1002115
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发表时间：
2015-04
期刊：
影响因子：
9.8
通讯作者：
Han J
中科院分区：
文献类型：
--
作者：
Hu W;Wang T;Wang X;Han J
在脊椎动物和无脊椎动物中，光感受器的输出由来自中间神经元的反馈信号调节，中间神经元有助于几种重要的视觉功能。虽然已知光感受器的突触反馈调节发生在果蝇中，但关于潜在的分子机制和生理实施的许多问题仍然不清楚。在这里，我们使用广泛的实验方法系统地研究了这些问题。我们分离出两个Ih突变的苍蝇线，表现出有节奏的光感受器去极化没有光刺激。我们发现Ih通道通过调节钙通道活性来调节无长突细胞谷氨酸的释放。此外，我们发现，眼富集红藻氨酸受体（EKAR）在光感受器中表达，并接收无长突细胞释放的谷氨酸信号。最后，我们提出的证据表明，无长突细胞的反馈调节有助于保持在环境光的光敏感性。我们的研究结果表明，从无长突细胞到光感受器的反馈调节的合理分子基础和生理效应。这些结果提供了新的机制洞察突触反馈调节如何通过调节神经信息传递和电路兴奋性参与网络处理。对果蝇视觉系统的系统研究阐明了无长突细胞对光感受器的反馈调节的分子机制和生理效应，这对维持光敏感性至关重要。反馈调节是神经回路在获取信息过程中的一个共同特征。因此，了解这种现象是如何发生的非常重要。以果蝇（Drosophila melanogaster）初级视觉系统为模型，系统研究了无长突细胞（存在于视皮层的二级神经元）对光感受器的反馈调节的分子机制和生理实现。我们分离出两个果蝇品系，其基因突变编码的离子通道称为Ih，其光感受器表现出有节奏的去极化在没有光刺激。我们证明，Ih通道在无长突细胞中发挥作用，通过调节电压门控钙通道Cac的活性来调节神经递质谷氨酸的释放。我们进一步发现，无长突细胞释放的谷氨酸信号是由光感受器表达的谷氨酸受体感受和转导的。最后，我们表明，这种反馈调节是至关重要的，在环境光的存在下保持光敏感性。我们的研究结果表明，在神经元网络的突触反馈调节调节信息传递和电路兴奋性。
In both vertebrates and invertebrates, photoreceptors’ output is regulated by feedback signals from interneurons that contribute to several important visual functions. Although synaptic feedback regulation of photoreceptors is known to occur in Drosophila, many questions about the underlying molecular mechanisms and physiological implementation remain unclear. Here, we systematically investigated these questions using a broad range of experimental methods. We isolated two Ih mutant fly lines that exhibit rhythmic photoreceptor depolarization without light stimulation. We discovered that Ih channels regulate glutamate release from amacrine cells by modulating calcium channel activity. Moreover, we showed that the eye-enriched kainate receptor (EKAR) is expressed in photoreceptors and receives the glutamate signal released from amacrine cells. Finally, we presented evidence that amacrine cell feedback regulation helps maintain light sensitivity in ambient light. Our findings suggest plausible molecular underpinnings and physiological effects of feedback regulation from amacrine cells to photoreceptors. These results provide new mechanistic insight into how synaptic feedback regulation can participate in network processing by modulating neural information transfer and circuit excitability. A systematic study of the Drosophila visual system clarifies the molecular mechanisms and physiological effects of feedback regulation of photoreceptors by amacrine cells, essential for maintaining light sensitivity. Feedback regulation is a common feature of neural circuits during the process of acquiring information. Therefore, it is important to understand how this phenomenon occurs. Using the primary visual system of the fruit fly Drosophila melanogaster as a model, we systematically investigated the molecular mechanisms and the physiological implementation of feedback regulation from amacrine cells (second order neurons that are present in the lamina) to photoreceptors. We isolated two fly lines with mutations in the gene that encodes for the ion channel known as Ih, whose photoreceptors exhibited rhythmic depolarizations in the absence of light stimulation. We demonstrated that Ih channels function in amacrine cells to regulate the release of the neurotransmitter glutamate by modulating the activity of the voltage-gated calcium channel, Cac. We further found that the glutamate signal released by amacrine cells is sensed and transduced by glutamate receptors expressed by the photoreceptors. Finally, we showed that this feedback regulation is critical for maintaining light sensitivity in the presence of ambient light. Our results suggest that regulation of synaptic feedback in a neuronal network modulates information transfer and circuit excitability.
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影响因子：
64.8
作者：
HARDIE, RC;PERETZ, A;MINKE, B
通讯作者：
MINKE, B
影响因子：
12.3
作者：
Cook RK;Christensen SJ;Deal JA;Coburn RA;Deal ME;Gresens JM;Kaufman TC;Cook KR
通讯作者：
Cook KR
影响因子：
5.5
作者：
Maccaferri, G;McBain, CJ
通讯作者：
McBain, CJ
DOI：
10.1126/stke.2202004pl6
发表时间：
2004-02-12
期刊：
Science's STKE : signal transduction knowledge environment
影响因子：
--
作者：
McGuire, Sean E;Mao, Zhengmei;Davis, Ronald L
通讯作者：
Davis, Ronald L
影响因子：
1.5
作者：
Hayashi, S;Ito, K;Goto, S
通讯作者：
Goto, S