Retinal bipolar cell input mechanisms in giant danio. II. Patch-clamp analysis of on bipolar cells.
Retinal bipolar cell input mechanisms in giant danio. II. Patch-clamp analysis of on bipolar cells.
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DOI：
10.1152/jn.00270.2004
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发表时间：
2005
影响因子：
2.5
通讯作者：
Kwoon Y. Wong;E. Cohen;J. Dowling
中科院分区：
文献类型：
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作者：
Kwoon Y. Wong;E. Cohen;J. Dowling
使用切片制剂通过全细胞膜片钳研究双极细胞上巨丹尼奥视网膜上的谷氨酸受体。从形态上识别了双极上的锥体驱动 (Cbs) 和双极上的混合输入 (Mbs)。大多数 Cbs 对兴奋性氨基酸转运蛋白 (EAAT) 底物 d-天冬氨酸有反应，但对 III 族代谢型谷氨酸受体 (mGluR) 激动剂 l-(+)-2-氨基-4-磷酸丁酸 (l-AP4) 或 AMPA/红藻氨酸受体激动剂红藻氨酸没有反应，表明 EAAT 是 Cbs 上的主要谷氨酸受体。 EAAT 抑制剂 dl-threo-beta-benzyloxyasparate (TBOA) 阻断 Cbs 的所有光诱发反应，表明这些反应完全由 EAAT 介导。相反，所有 Mb 对 d-天冬氨酸和 l-AP4 有反应，但对红藻氨酸没有反应，表明它们同时具有 EAAT 和 III 组 mGluR（可能是 mGluR6）。 Mb 的光反应涉及两种受体，因为它们可以被 TBOA 加 (RS)-α-环丙基-4-膦酰基苯基甘氨酸（CPPG，III 组 mGluR 拮抗剂）阻断，但不能单独被其中任何一种受体阻断。在暗适应条件下，CPPG 降低了 Mbs 对绿色（视杆选择性）刺激的反应，但 TBOA 增强了 Mbs 对绿色（视杆选择性）刺激的反应。相比之下，尽管 TBOA 更有效，但两种拮抗剂均降低了对红色（视锥细胞选择性）刺激的反应。此外，在明视条件下，TBOA未能消除Mbs的光诱发反应。因此，在 Mbs 上，视杆细胞输入主要由 mGluR6 介导，而视锥细胞输入主要由 EAAT 介导，但在某种程度上也由 mGluR6 介导。最后，我们探讨了 EAAT 和 Mbs 中 mGluR6 之间的相互作用。 l-AP4 降低了对 d-天冬氨酸的反应，反之亦然。因此，mGluR6 和 EAAT 相互抑制，这可能是 Mbs 中杆状信号和锥状信号之间相互抑制的基础。
Glutamate receptors on giant danio retinal on bipolar cells were studied with whole cell patch clamping using a slice preparation. Cone-driven on bipolars (Cbs) and mixed-input on bipolars (Mbs) were identified morphologically. Most Cbs responded to the excitatory amino acid transporter (EAAT) substrate d-aspartate but not to the group III metabotropic glutamate receptor (mGluR) agonist l-(+)-2-amino-4-phosphonobutyric acid (l-AP4) or the AMPA/kainate receptor agonist kainate, suggesting EAATs are the primary glutamate receptors on Cbs. The EAAT inhibitor dl-threo-beta-benzyloxyasparate (TBOA) blocked all light-evoked responses of Cbs, suggesting these responses are mediated exclusively by EAATs. Conversely, all Mbs responded to d-aspartate and l-AP4 but not to kainate, indicating they have both EAATs and group III mGluRs (presumably mGluR6). The light responses of Mbs involve both receptors because they could be blocked by TBOA plus (RS)-alpha-cyclopropyl-4-phosphonophenylglycine (CPPG, a group III mGluR antagonist) but not by either alone. Under dark-adapted conditions, the responses of Mbs to green (rod-selective) stimuli were reduced by CPPG but enhanced by TBOA. In contrast, both antagonists reduced the responses to red (cone-selective) stimuli, although TBOA was more effective. Furthermore, under photopic conditions, TBOA failed to eliminate light-evoked responses of Mbs. Thus on Mbs, rod inputs are mediated predominantly by mGluR6, whereas cone inputs are mediated mainly by EAATs but also by mGluR6 to some extent. Finally, we explored the interactions between EAATs and mGluR6 in Mbs. Responses to d-aspartate were reduced by l-AP4 and vice versa. Therefore mGluR6 and EAATs suppress each other, and this might underlie mutual suppression between rod and cone signals in Mbs.