Pardue Machelle T, Phillips Michael J, Yin Hang, Sippy Brian D, Webb-Wood Sarah, Chow Alan Y, Ball Sherry L
Atlanta VA Medical Center, Decatur, GA 30033, USA.
Invest Ophthalmol Vis Sci. 2005 Feb;46(2):674-82. doi: 10.1167/iovs.04-0515.
Retinal prosthetics have been designed to interface with the neural retina by electrically stimulating the remaining retinal circuits after photoreceptor degeneration. However, the electrical stimulation provided by the subretinal implant may also stimulate neurotrophic factors that provide neuroprotection to the retina. This study was undertaken to determine whether electrical stimulation from a subretinal photodiode-based implant has a neuroprotective effect on photoreceptors in the RCS rat, a model of photoreceptor degeneration.
Eyes of RCS rats were implanted with an active or inactive device or underwent sham surgery before photoreceptor degeneration. Outer retinal function was assessed with electroretinogram (ERG) recordings weekly until 8 weeks after surgery, at which time retinal tissue was collected and processed for morphologic assessment, including photoreceptor cell counts and retinal layer thickness.
At 4 to 6 weeks after surgery, the ERG responses in the active-implant eyes were 30% to 70% greater in b-wave amplitude than the responses from eyes implanted with inactive devices, those undergoing sham surgery, or the nonsurgical control eyes. At 8 weeks after surgery the ERG responses from active-implant eyes were not significantly different from the control groups. However, the number of photoreceptors in eyes implanted with the active or inactive device was significantly greater in the regions over and around the implant versus sham-surgical and nonsurgical control eyes.
These results suggest that subretinal electrical stimulation provides temporary preservation of retinal function in the RCS rat. In addition, implantation of an active or inactive device into the subretinal space causes morphologic preservation of photoreceptors in the RCS rat until 8 weeks after surgery. Further studies are needed to determine whether the correlation of neuropreservation with subretinal implantation is due to electrical stimulation and/or a mechanical presence of the implant in the subretinal space.
视网膜假体的设计旨在通过在光感受器退化后电刺激剩余的视网膜回路与神经视网膜建立连接。然而,视网膜下植入物提供的电刺激也可能刺激为视网膜提供神经保护的神经营养因子。本研究旨在确定基于视网膜下光电二极管的植入物产生的电刺激对光感受器退化模型RCS大鼠的光感受器是否具有神经保护作用。
在光感受器退化之前,给RCS大鼠的眼睛植入有源或无源装置,或进行假手术。每周用电视网膜图(ERG)记录评估视网膜外层功能,直至术后8周,此时收集视网膜组织并进行形态学评估,包括光感受器细胞计数和视网膜层厚度。
术后4至6周,有源植入眼的ERG反应b波振幅比植入无源装置的眼、接受假手术的眼或未手术对照眼的反应大30%至70%。术后8周,有源植入眼的ERG反应与对照组无显著差异。然而,与假手术和未手术对照眼相比,植入有源或无源装置的眼中,植入物上方及周围区域的光感受器数量明显更多。
这些结果表明,视网膜下电刺激可使RCS大鼠的视网膜功能得到暂时保留。此外,在视网膜下间隙植入有源或无源装置可使RCS大鼠的光感受器在术后8周内保持形态完整。需要进一步研究来确定神经保护与视网膜下植入的相关性是否归因于电刺激和/或植入物在视网膜下间隙的机械存在。