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Neural mechanism of lateral inhibition in the retina

视网膜侧抑制的神经机制

基本信息

批准号：
14380378
负责人：
KANEKO Akimichi
金额：
$ 9.02万
依托单位：
Seijoh University (2003-2004)Keio University (2002)
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
2002
资助国家：
日本
起止时间：
2002 至 2004
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-14380378/
关键词：
Receptive field Lateral inhibition Horizontal cell Cone photoreceptor Calcium current pH Retina 網膜錐体子細胞

项目摘要

The feedback mechanism from horizontal cells to cone photoreceptors was investigated by the whole cell patch clamp recording from cones in newt retinal slices. GABA-mediated effect has been removed by 100μM picrotoxin. Illumination of the receptive field surround evoked depolarization in cones and shifted the activation voltage of cone calcium current (I_<Ca>) to negative voltages. This effect appeared similar to what was reported by Verweij et al. (1996) as field effect, but the shift of the current-voltage (I-V) relation of I_<Ca> was not merely the parallel shift along the voltage axis as expected for the field effect, because surround illumination increased Ica even at the voltages more positive than I_<Ca> peak. Focal application of high pH solution to the cone terminal layer increased I_<Ca> in a similar manner as the surround illumination. These observations suggest a possibility that surround illumination lowered the proton concentration in the cone terminal region. In fact, enrichment of the pH buffering capacity of extracellular solution by adding 10mM HEPES or 15mM Tris to the bicarbonate buffer increased I_<Ca>, in which additional I_<Ca> increase by surround illumination was not seen. CNQX hyperpolarized horizontal cells (HCs) and augmented cone I_<Ca>. Kainate depolarized HCs and suppressed cone I_<Ca>. Surround responses of cones were not seen in the presence of either kainite or CNQX. Therefore, it is highly likely that cone I_<Ca> is intimately related to the membrane voltage of HCs. From the present results we propose that an external proton mediates feedback for surround inhibition in the outer retina. The mechanisms regulating proton concentration in relation to HC membrane voltage needs to be elucidated.

在Newt视网膜薄片上，用全细胞膜片钳记录水平细胞对视锥感光细胞的反馈机制。γ-氨基丁酸介导的作用已被100μM印防己毒素所消除。照射感受野可引起视锥细胞去极化，并使视锥细胞钙电流的激活电压(I&lt；Ca&gt；)移至负电压。这一效应似乎与Verweij等人的报告相似。(1996)的场效应，但电流-电压(I-V)关系的移动不仅仅是场效应所预期的沿电压轴的平行移动，因为即使在比I&lt；Ca&gt；峰值更正的电压下，周围照明也会增加Ica。在圆锥体末端层集中施加高pH溶液，与周围光照的方式相似，增加了I_lt；Ca&gt；。这些观测结果表明，环绕光可能降低了锥体终端区的质子浓度。事实上，在碳酸氢盐缓冲液中加入10 mM HEPES或15 mM Tris可提高胞外液的pH缓冲能力，但并未观察到环境光照对胞外液pH缓冲能力的影响。CNQX超极化水平细胞(HCS)和增强型锥体细胞。海人藻酸盐使Hcs去极化，抑制锥体i&lt；Ca&gt；无论是在海藻土或CNQX存在下，都没有观察到圆锥体的环绕反应。因此，锥体I&lt；Ca&gt；很可能与HCS的膜电压密切相关。从目前的结果我们认为，一个外部的质子中介反馈的环绕抑制在视网膜外部。与HC膜电压有关的调节质子浓度的机制需要阐明。