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脱离性视网膜病变对视锥突触的损伤：与视杆突触的差异和 ROCK 抑制的保护作用。

Injury to Cone Synapses by Retinal Detachment: Differences from Rod Synapses and Protection by ROCK Inhibition.

机构信息

Department of Pharmacology, Physiology and Neuroscience, Rutgers New Jersey Medical School, 185 South Orange Avenue, Newark, NJ 07103, USA.

Institute of Ophthalmology and Visual Science, Rutgers New Jersey Medical School, 90 Bergen Street, Newark, NJ 07103, USA.

出版信息

Cells. 2023 May 27;12(11):1485. doi: 10.3390/cells12111485.

DOI:10.3390/cells12111485
PMID:37296606
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10253016/
Abstract

Attachment of a detached retina does not always restore vision to pre-injury levels, even if the attachment is anatomically successful. The problem is due in part to long-term damage to photoreceptor synapses. Previously, we reported on damage to rod synapses and synaptic protection using a Rho kinase (ROCK) inhibitor (AR13503) after retinal detachment (RD). This report documents the effects of detachment, reattachment, and protection by ROCK inhibition on cone synapses. Conventional confocal and stimulated emission depletion (STED) microscopy were used for morphological assessment and electroretinograms for functional analysis of an adult pig model of RD. RDs were examined 2 and 4 h after injury or two days later when spontaneous reattachment had occurred. Cone pedicles respond differently than rod spherules. They lose their synaptic ribbons, reduce invaginations, and change their shape. ROCK inhibition protects against these structural abnormalities whether the inhibitor is applied immediately or 2 h after the RD. Functional restoration of the photopic b-wave, indicating cone-bipolar neurotransmission, is also improved with ROCK inhibition. Successful protection of both rod and cone synapses with AR13503 suggests this drug will (1) be a useful adjunct to subretinal administration of gene or stem cell therapies and (2) improve recovery of the injured retina when treatment is delayed.

摘要

视网膜脱离的附着并不总是能使视力恢复到受伤前的水平，即使附着在解剖上是成功的。这个问题部分是由于光感受器突触的长期损伤。以前，我们报道了在用 Rho 激酶（ROCK）抑制剂（AR13503）治疗视网膜脱离（RD）后，杆状突触和突触保护的损伤。本报告记录了脱离、再附着和 ROCK 抑制对锥体突触的保护作用。使用传统共焦和受激发射损耗（STED）显微镜进行形态评估，并用成年猪 RD 模型进行视网膜电图功能分析。在损伤后 2 小时和 4 小时或自发再附着后两天检查 RD。与杆状小体不同，锥体足细胞失去了它们的突触带，减少了内陷，并改变了它们的形状。ROCK 抑制可以防止这些结构异常，无论抑制剂是在 RD 后立即应用还是 2 小时后应用。用 ROCK 抑制也能改善光感受器 b 波的功能恢复，表明锥体-双极神经传递得到改善。用 AR13503 成功保护杆状和锥体突触表明，这种药物将：（1）作为视网膜下基因或干细胞治疗的辅助手段非常有用；（2）当治疗延迟时，改善受伤视网膜的恢复。

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