Margetts Megan, Rufus-Toye Remi, Jiang Xiaofan, Leo Shaun M, Chow Isabelle, Indusegaran Mathura, Hysi Pirro G, Webster Andrew R, Hammond Christopher J, Mahroo Omar A
Physiology, Development & Neuroscience, University of Cambridge, Cambridge, United Kingdom.
Institute of Ophthalmology, University College London, London, United Kingdom.
Invest Ophthalmol Vis Sci. 2025 Sep 2;66(12):30. doi: 10.1167/iovs.66.12.30.
The purpose of this study was to explore whether nyctalopia in vitamin A deficiency (VAD) is attributable to simple reduction in quantal catch or to an "equivalent background" phenomenon.
Five individuals were recruited for experimental electroretinograms (ERGs), including three healthy participants (aged 21 to 47 years), one patient with VAD (aged 70 years), and one patient with GNAT2-associated achromatopsia (aged 43 years). Recordings used conductive fiber electrodes and followed dark adaptation and mydriasis. Dim flashes of varying strengths were delivered in the dark to mimic reduction in quantal catch; flashes of fixed strength (0.03 scotopic cd·s/m2) were delivered on dim blue backgrounds.
International standard recordings in the patient with VAD showed selective attenuation of dark-adapted responses in severe deficiency, which normalized following treatment. Light-adapted responses did not change. In experimental recordings, both reducing flash strength and applying dim backgrounds reduced ERG amplitude. Reducing flash strength also increased latency of the response, whose rising phase and peak became progressively delayed. Dim backgrounds did not prolong latency. This was seen in all participants, including the patient with achromatopsia, indicating that this was a property of the rod system. In moderate VAD, the dim-flash response was reduced, but not delayed, resembling the response seen in the presence of a dim background.
Our findings indicate that rod system desensitization in VAD likely arises from an "equivalent background" effect, probably arising from activation of phototransduction by free opsin. Activation to a similar degree is known not to occur in cones, helping explain why VAD selectively affects night vision.
本研究旨在探讨维生素A缺乏(VAD)导致的夜盲是由于量子捕获量简单减少还是“等效背景”现象所致。
招募了5名个体进行实验性视网膜电图(ERG)检查,包括3名健康参与者(年龄21至47岁)、1名VAD患者(70岁)和1名与GNAT2相关的全色盲患者(43岁)。记录采用导电纤维电极,并遵循暗适应和散瞳程序。在黑暗中给予不同强度的暗光闪烁以模拟量子捕获量的减少;在昏暗的蓝色背景上给予固定强度(0.03 scotopic cd·s/m2)的闪光。
VAD患者的国际标准记录显示,在严重缺乏时,暗适应反应有选择性衰减,治疗后恢复正常。明适应反应未改变。在实验记录中,降低闪光强度和应用昏暗背景均降低了ERG振幅。降低闪光强度还增加了反应的潜伏期,其上升相和峰值逐渐延迟。昏暗背景未延长潜伏期。在所有参与者中均观察到这一现象,包括全色盲患者,表明这是视杆系统的特性。在中度VAD中,暗光闪烁反应降低但未延迟,类似于在存在昏暗背景时观察到的反应。
我们的研究结果表明,VAD中视杆系统脱敏可能源于“等效背景”效应,可能是由游离视蛋白激活光转导引起的。已知在视锥细胞中不会发生类似程度的激活,这有助于解释为什么VAD选择性地影响夜间视力。