Abstract：
Nearly all modern life depends on artificial light; however, it does cause health problems. With certain restrictions of artificial light emitting technology, the influence of the light spectrum is inevitable. The most remarkable problem is its overload in the short wavelength component. Short wavelength artificial light has a wide range of influences from ocular development to mental problems. The visual neuronal pathway, as the primary light-sensing structure, may contain the fundamental mechanism of all light-induced abnormalities. However, how the artificial light spectrum shapes the visual neuronal pathway during development in mammals is poorly understood. We placed C57BL/6 mice in three different spectrum environments (full-spectrum white light: 400-750 nm; violet light: 400 ± 20 nm; green light: 510 ± 20 nm) beginning at eye opening, with a fixed light time of 7:00-19:00. During development, we assessed the ocular axial dimension, visual function and retinal neurons. After two weeks under short wavelength conditions, the ocular axial length (AL), anterior chamber depth (ACD) and length of lens thickness, real vitreous chamber depth and retinal thickness (LLVR) were shorter, visual acuity (VA) decreased, and retinal electrical activity was impaired. The density of S-cones in the dorsal and ventral retinas both decreased after one week under short wavelength conditions. In the ventral retina, it increased after three weeks. Retinal ganglion cell (RGC) density and axon thickness were not influenced; however, the axonal terminals in the lateral geniculate nucleus (LGN) were less clustered and sparse. Amacrine cells (ACs) were significantly more activated. Green light has few effects. The KEGG and GO enrichment analyses showed that many genes related to neural circuitry, synaptic formation and neurotransmitter function were differentially expressed in the short wavelength light group. In conclusion, exposure to short wavelength artificial light in the early stage of vision-dependent development in mice delayed the development of the visual pathway. The axon terminus structure and neurotransmitter function may be the major suffering.
摘要：
几乎所有的现代生活都依赖于人造光；然而，它确实会引起健康问题。由于人工发光技术的某些限制,光谱的影响是不可避免的。最显著的问题是其在短波长分量中的过载。短波长人造光具有从眼部发育到精神问题的广泛影响。视觉神经元通路，作为主要的光敏结构，可能包含所有光致异常的基本机制。然而,在哺乳动物的发育过程中，人工光谱如何塑造视觉神经元通路还知之甚少。我们从睁眼开始将C57BL/6小鼠置于三种不同的光谱环境中（全光谱白光：400-750nm；紫光：400±20nm；绿光：510±20nm），固定照明时间为7:00-19:00。在开发过程中,我们评估了眼轴尺寸，视觉功能和视网膜神经元。在短波长条件下两周后，眼轴长度（AL），前房深度（ACD）和晶状体厚度长度，真实玻璃体腔深度和视网膜厚度（LLVR）较短，视力（VA）下降，视网膜电活动受损。在短波长条件下一周后，背侧和腹侧视网膜中的S锥密度均降低。在腹侧视网膜，三周后增加。视网膜神经节细胞（RGC）密度和轴突厚度不受影响；然而，外侧膝状核（LGN）的轴突末端较少聚集和稀疏。无极细胞(AC)显著更活化。绿灯几乎没有影响。KEGG和GO富集分析表明，许多与神经回路相关的基因，短波组突触形成和神经递质功能差异表达。总之,在小鼠视觉依赖性发育的早期阶段暴露于短波长人造光会延迟视觉通路的发育。轴突末端结构和神经递质功能可能是主要的痛苦。
