Ostrin Lisa A
College of Optometry, University of Houston, Houston, USA.
Ophthalmic Physiol Opt. 2018 Sep;38(5):503-515. doi: 10.1111/opo.12583. Epub 2018 Sep 26.
The intrinsically photosensitive retinal ganglion cells (ipRGCs) signal environmental light, control pupil size and entrain circadian rhythm. There is speculation that ipRGCs may be involved in the protective effects of light exposure in myopia. Here, the ipRGC-driven pupil response was evaluated in children and examined with light exposure and refractive error.
Children ages 5-15 years participated. Subjects wore an actigraph device prior to the lab visit for objective measures of light exposure and sleep. For pupillometry, the left eye was dilated and presented with stimuli, and the consensual pupil response was measured in the right eye. Pupil measurements were preceded by 5 min dark adaptation. In Experiment 1 (n = 14), 1 s long wavelength light ('red,' 651 nm, 167 cd m ) and 10 increasing intensities of 1 s short wavelength light ('blue,' 456 nm, 0.167-167 cd m ) were presented with a 60 s interstimulus interval. A piecewise two-segment regression was fit to the stimulus response function to determine the functional melanopsin threshold. Pupil responses were analysed with light exposure over the previous 24 h. For Experiment 2 (n = 42), three 1 s red and three 1 s blue alternating stimuli were presented with a 60 s interstimulus interval. Following an additional 5-min dark adaption, the experiment was repeated. Pupil metrics included peak constriction, the 6 s and 30 s post-illumination response (PIPR), early and late area under the curve (AUC). Following pupil measurements, cycloplegic refractive error and axial length were measured.
For Experiment 1, PIPR metrics demonstrated a graded response to increasing intensity blue stimuli, with a mean functional melanopsin threshold of 6.2 ± 4.5 cd m (range: 0.84-16.7 cd m ). The 6 s PIPR and early AUC were associated with 24-h light exposure for high intensity stimuli (33.3 and 83.3 cd m , p < 0.005 for both). For Experiment 2, there were no associations between pupil metrics and refractive error. The 6 s PIPR and early AUC to blue stimuli were significantly increased for Trial 2 compared to Trial 1.
The ipRGC-driven pupil responses in children were robust and similar to responses previously measured in an adult population. The 6 s PIPR and early AUC to high intensity blue stimuli were associated with previous light exposure. There were no associations between the ipRGC-driven pupil response and refractive status in this cohort.
内在光敏性视网膜神经节细胞(ipRGCs)传递环境光信号,控制瞳孔大小并调节昼夜节律。有人推测,ipRGCs可能参与了光照对近视的保护作用。在此,我们评估了儿童中由ipRGCs驱动的瞳孔反应,并研究了光照暴露和屈光不正与之的关系。
5至15岁的儿童参与了研究。受试者在实验室检查前佩戴活动记录仪,以客观测量光照暴露和睡眠情况。进行瞳孔测量时,左眼散瞳并接受刺激,同时测量右眼的交感瞳孔反应。瞳孔测量前先进行5分钟的暗适应。在实验1(n = 14)中,以60秒的刺激间隔呈现1秒的长波长光(“红色”,651纳米,167坎德拉/平方米)和10种强度递增的1秒短波长光(“蓝色”,456纳米,0.167 - 167坎德拉/平方米)。对刺激反应函数进行分段两段回归拟合,以确定功能性黑视蛋白阈值。根据前24小时的光照暴露情况分析瞳孔反应。在实验2(n = 42)中,以60秒的刺激间隔交替呈现三个1秒的红色和三个1秒的蓝色刺激。在额外进行5分钟暗适应后,重复该实验。瞳孔指标包括最大收缩、光照后6秒和30秒反应(PIPR)、曲线下早期和晚期面积(AUC)。瞳孔测量后,测量睫状肌麻痹后的屈光不正和眼轴长度。
对于实验1,PIPR指标显示对强度增加的蓝色刺激有分级反应,功能性黑视蛋白平均阈值为6.2±4.5坎德拉/平方米(范围:0.84 - 16.7坎德拉/平方米)。高强度刺激(33.3和83.3坎德拉/平方米)下,6秒PIPR和早期AUC与24小时光照暴露相关(两者p均<0.005)。对于实验2,瞳孔指标与屈光不正之间无关联。与实验1相比,实验2中蓝色刺激的6秒PIPR和早期AUC显著增加。
儿童中由ipRGCs驱动的瞳孔反应强烈,与先前在成人中测量的反应相似。高强度蓝色刺激下的6秒PIPR和早期AUC与先前的光照暴露相关。在该队列中,由ipRGCs驱动的瞳孔反应与屈光状态之间无关联。