RXRα对正常及形觉剥夺豚鼠屈光状态及眼球生长的调控

目的 通过对豚鼠球旁注射RXRα激动剂或抑制剂,研究RXRα在正常及形觉剥夺豚鼠屈光状态及眼球生长方面的调控作用,从而明确RXRα在屈光发育和近视形成中的作用.方法 实验研究.将245只正常3周龄体质量在100 g左右的三色豚鼠245只,采用直接抽样法分为正常组和形觉剥夺(FDM)组,2组又各分为空白对照组、溶剂组和给药组.溶剂组和给药组豚鼠每天右眼球旁分别注射DMSO或RXRα激动剂Fluorobexarotene或RXRα抑制剂HX531,连续注射4周,对侧眼不做处理.实验前和实验后2、4周分别检测屈光度和眼轴参数.正常组在实验结束后免疫荧光检测巩膜RXRα含量.采用独立样本t检验和单因素方差分析进行数据分析.结果 球旁注射Fluorobexarotene 4周后,豚鼠巩膜RXRα表达增加;球旁注射HX531 4周后,巩膜RXRα表达减少.不论注射RXRα激动剂或是抑制剂,正常组及形觉剥夺组豚鼠屈光状态和眼轴参数变化差异均无统计学意义.结论 球旁注射RXRα激动剂Fluorobexarotene或抑制剂HX531对正常及形觉剥夺豚鼠屈光发育及眼球生长无明显影响,提示单独RXRα对正常以及FDM豚鼠的屈光发育和眼球生长可能没有直接调控作用.     

单眼剥夺幼猫眼球轴长和屈光度的动态变化

目的研究视觉发育关键期单眼剥夺幼猫眼轴轴长及屈光状态的变化。方法动态计录了１５只健康和１８只单眼眼睑缝合幼猫眼轴长度和屈光状态的变化。结果剥夺眼较伴随眼眼轴增长。剥夺时间越长，眼轴增长越明显。１６周龄猫剥夺眼平均眼球轴长１６．２７±２．２８ｍｍ，与伴随眼比较（Ｐ＝０．００３）。屈光状态趋于正视，但眼轴增长与屈光值间无一致关系。结论形觉剥夺导致眼球眼轴增长和近视。结果进一步支持视觉剥夺影响眼球发育的学说。     

左旋多巴对豚鼠形觉剥夺性近视形成的影响

目的研究腹腔注射左旋多巴（L-dopa）对豚鼠形觉剥夺性近视眼屈光状态及视网膜多巴胺含量的影响。方法眼罩遮盖建立豚鼠形觉剥夺性近视眼模型,分为正常对照组、L—dopa组（10mg／kg）、生理盐水组、遮盖组、遮盖＋L-dopa组、遮盖＋生理盐水组6个组。遮盖10d后,测定角膜曲率半径、眼球屈光度和眼轴长度,高效液相色谱检测视网膜多巴胺含量。结果眼罩遮盖10d后,豚鼠遮盖眼眼轴延长、近视形成,视网膜多巴胺含量降低（P〈0．05）,但角膜曲率半径无明显变化。腹腔注射L-dopa引起遮盖眼视网膜多巴胺含量增加、近视程度减轻（P〈0．05）,但对正常豚鼠眼球的屈光发育无明显影响（P〉0．05）。腹腔注射生理盐水后,豚鼠眼球屈光状态和视网膜多巴胺含量无明显变化（P〉0．05）。结论腹腔注射L—dopa能通过补充遮盖眼视网膜多巴胺含量,抑制豚鼠形觉剥夺性近视的形成。     

PPARy受体激动剂罗格列酮对形觉剥夺性近视和正常豚鼠屈光度的影响

目的　探讨过氧化物酶体增殖物激活受体y（PPARy）激动剂罗格列酮在豚鼠形觉剥夺性近视（FDM）中的作用。方法　选取40只3周龄豚鼠（均为右眼）,随机分成4组:正常组、FDM组、正常+罗格列酮组、FDM+罗格列酮组,其中正常组豚鼠不做处理,FDM组豚鼠使用头套法造模,正常+罗格列酮组豚鼠每天腹腔注射罗格列酮5 mg·kg^-1,FDM+罗格列酮组豚鼠每天戴头套并腹腔注射罗格列酮5 mg·kg^-1,持续28 d。实验前和实验后28 d测量豚鼠屈光度,实验后28 d测量豚鼠眼轴长度,保留眼球,免疫组织化学及Western blot测量豚鼠I型胶原蛋白(COL-I)、转化生长因子-β1（TGF-β1）、基质金属蛋白酶-2（MMP-2）、基质金属蛋白酶抑制剂-2（TIMP-2）蛋白的分布与表达,HE染色观察巩膜形态变化。结果　与正常组相比,FDM组豚鼠右眼屈光度和眼轴长度均增加,形成相对近视,差异均有统计学意义（均为P<0.05）;巩膜明显变薄,胶原纤维排列紊乱,断裂明显,分布不规则。与正常组相比,正常+罗格列酮组豚鼠右眼屈光度和眼轴长度变化差异均无统计学意义（均为P>0.05）;巩膜形态没有明显变化。与正常组相比,FDM+罗格列酮组豚鼠右眼屈光度和眼轴长度变化差异均无统计学意义（均为P>0.05）。与FDM组相比,FDM+罗格列酮组豚鼠右眼屈光度和眼轴长度均减少,差异均有统计学意义（均为P<0.05）;巩膜胶原纤维排列松散,分布略紊乱。Western blot检测结果显示,与正常组相比,FDM组豚鼠巩膜中COL-I、TGF-β1、TIMP-2蛋白表达量均减少,MMP-2蛋白表达量增加,差异均有统计学意义（均为P<0.05）;与正常组相比,正常+罗格列酮组豚鼠巩膜中,COL-I、TGF-β1蛋白表达量均增加,差异均有统计学意义（均为P<0.05）,TIMP-2和MMP-2蛋白表达量差异均无统计学意义（均为P>0.05）;与正常组相比,FDM+罗格列酮组豚鼠巩膜中COL-I蛋白的表达接近正常组,差异无统计学意义（P>0.05）,TGF-β1、TIMP-2蛋白表达量均增加,MMP-2蛋白表达量减少,差异均有统计学意义（均为P<0.05）;与FDM组相比,FDM+罗格列酮组豚鼠巩膜中COL-I、TGF-β1、TIMP-2蛋白表达量均增加,MMP-2蛋白表达量减少,差异均有统计学意义（均为P<0.05）。豚鼠巩膜中COL-I、TGF-β1、TIMP-2、MMP-2蛋白免疫组织化学表达趋势与Western blot检测结果一致。结论　PPARy受体激动剂罗格列酮可能通过调节TGF-β1、COL-I、TIMP-2和MMP-2蛋白的表达水平抑制FDM,对正常豚鼠的屈光影响不大。     

C57BL/6小鼠形觉剥夺性近视动物模型的建立

目的 探讨C57BL/6小鼠形觉剥夺性近视与眼球生物学参数的变化,揭示小鼠实验性近视形成的敏感期,以及形觉剥夺对小鼠屈光发育的影响.方法 实验研究.23日龄C57BL/6小鼠74只,随机分为3组,单眼形觉剥夺组:剥夺2周(n=12)、3周(n=20)和4周(n=18),对侧眼作为自身对照;形觉剥夺恢复组(n=10):单眼形觉剥夺4周,分别恢复4 d和7 d;正常对照组(n=14).实验前后分别用红外偏心摄影验光仪测量小鼠眼球的屈光状态,修正过的人眼角膜曲率计测量角膜曲率半径,相干光断层扫描仪测量眼球生物学参数,包括眼前节、晶状体厚度、玻璃体腔深度和眼轴长度等.对组内实验眼和对侧眼的屈光力、角膜曲率半径、眼球参数的比较采用配对t检验,不同组间比较采用独立样本t检验进行统计学分析.结果 形觉剥夺2周,实验眼相比对侧眼向近视方向漂移(-0.85±1.65)D,眼球各生物学参数未见明显改变;形觉剥夺3周,实验眼相比对照眼向近视方向漂移(-4.27±1.60)D(t=-1.72,P=0.095);形觉剥夺4周组,实验眼相比对侧眼向近视方向漂移(-5.27±1.28)D(t=-2.64,P<0.05)并伴玻璃体腔深度延长(27±13)μm和眼轴长度增加(28±12)μm;上除眼罩7 d,实验性近视完全恢复.结论 小鼠单眼形觉剥夺4周可诱导出相对近视,但诱导时间较其他近视动物模型长;去除眼罩7 d,实验性近视完全恢复;利用相干光断层扫描仪测最小鼠眼球生物学参数可以较好反映屈光度的改变.     

Smad1在C57BL/6小鼠形觉剥夺性近视中的作用机制

目的：：通过建立C57 BL/6小鼠形觉剥夺性近视模型,探究Smad1在近视形成中的作用机制。方法：将60只3周龄C57 BL/6小鼠随机分为实验组和正常对照组(NC),包括形觉剥夺3wk组(FDM 3W,n=20),形觉剥夺4wk组(FDM 4W,n=20),FDM3W正常对照组(FDM 3W-NC,n=10)和FDM4W正常对照组(FDM 4W-NC,n=10),实验组右眼遮盖,左眼自然暴露作为自身对照,正常对照组不予任何处理。在实验3 wk及4 wk时检测所有小鼠屈光状态,HE染色观察巩膜及视网膜组织结构变化,免疫组织化学方法及实时荧光定量PCR观察Smad1在视网膜中的表达情况。结果：(1)自身对照眼和正常对照组呈生理性远视化发展,FDM3W、FDM4W实验眼均呈相对近视化发展,差异具有统计学意义(P<0.05);(2)与自身对照组及正常对照组比较,FDM3W、FDM4W实验眼巩膜及视网膜明显变薄;实验眼视网膜中Smad1表达明显下降,差异具有显著统计学意义(P<0.01)。结论：小鼠形觉剥夺性近视眼视网膜(尤其是内核层及内丛状层)中Smad1的表达呈下调趋势, Smad1极有可能通过转导视网膜信号参与了近视发生发展过程。     

BMP-2在C57BL/6小鼠形觉剥夺性近视眼巩膜中表达的变化

目的:观察C57BL/6小鼠形觉剥夺性近视(form deprivation myopia,FDM)巩膜中BMP-2表达的变化,研究其在巩膜重塑中发挥的作用.方法:选择3～4周龄的C57BL/6小鼠64只,以随机数字表法随机分为形觉剥夺21d组(16只)、同龄对照组(16只);形觉剥夺28d组(16只)、同龄对照组(16只).形觉剥夺前后对所有小鼠进行带状光剪影验光检测小鼠眼球的屈光状态,游标卡尺测量小鼠的眼轴长度,造模后分别于21d和28d取小鼠的巩膜组织,苏木素-伊红(HE)染色观察小鼠巩膜组织形态学变化,用荧光定量RT-PCR和免疫组织化学检测各组小鼠巩膜BMP-2 mRNA和其蛋白的表达水平.结果:小鼠形觉剥夺21d和28d后,剥夺眼分别诱导出-1.60±1.03D和-3.10±1.19D的相对近视,眼轴分别拉长16±12μm和21±13μm,与自身对照组和正常对照相比较,差异有统计学意义(P＜0.05).HE染色行巩膜形态学观察,可观察到剥夺眼巩膜变薄,胶原纤维排列紊乱.荧光定量RT-PCR和免疫组织化学结果显示实验眼BMP-2mRNA和蛋白的表达明显下调,与自身对照和正常对照组相比差异有统计学意义(P＜0.05).结论:C57 BL/6小鼠形觉剥夺眼巩膜中BMP-2呈下调趋势,BMP-2可能参与了近视发展过程中的巩膜重塑作用,其具体机制有待进一步研究.     

姜黄素在三色豚鼠近视发生发展中的作用

目的研究姜黄素在三色豚鼠近视发展中的作用。方法实验研究。将111只正常三色豚鼠（3周龄）随机分为正常给药组（N）和形觉剥夺组（FDM）两大组,每大组又分为空白对照组（N：n=13,FDM：n=12）、溶剂对照组（N：n=13,FDM：n=13）和姜黄素给药组（低剂量组15 µg;N：n=17,FDM：n=17;高剂量组150 µg;N：n=15,FDM：n=15）。其中溶剂对照组每天球旁注射二甲基亚枫（DMSO） 100 µl（10%）,姜黄素给药组每天球旁注射相应剂量姜黄素100 µl。实验前、实验后2周和4周分别检测屈光度、眼轴等参数。实验2周后,采用Western Blot方法检测巩膜胶原蛋白表达量。屈光度、眼球相关参数组内双眼间比较采用配对t检验,组间比较采用单因素方差分析（Bonferroni校正）。结果实验前,各组间的屈光度和眼轴等参数差异均无统计学意义。空白对照组和溶剂对照组的屈光度和眼轴等参数在实验前后各时间点差异也无统计学意义。注射4周后,姜黄素剂量依赖性诱导正常豚鼠产生近视 [N+DMSO组vs. N+15 µg组 vs. N+150 µg组：（-0.37±0.38）D vs. （-1.62±1.63）D vs. （-3.90±1.79）D,F=21.510,P＜0.001],并伴有眼轴延长[N+DMSO组vs. N+15 µg组 vs. N+150 µg组：（0.01±0.03）mm vs. （0.04±0.05）mm vs. （0.07±0.06）mm,F=4.992,P=0.011]。同时姜黄素加剧了豚鼠形觉剥夺性近视 [FDM+DMSO组 vs. FDM+15 µg组 vs. FDM+150 µg组：（-7.81±3.24）D vs. （-8.99±3.12）D vs. （-10.93±1.96）D,F=4.425,P=0.018],眼轴有相应延长,但差异无统计学意义。同时,姜黄素150 µg注射眼巩膜胶原蛋白Ⅰ的表达量下降（对侧眼vs.处理眼：0.33±0.08 vs. 0.18±0.03,t=-2.305,P=0.043）。结论姜黄素能诱导正常豚鼠出现近视并加剧形觉剥夺性近视,其机制可能是通过降低巩膜内的胶原含量。     

C57BL／6小鼠形觉剥夺性近视巩膜COLlσ2启动子区域CpG岛甲基化水平

目的研究C57BL／6小鼠形觉剥夺性近视形成和恢复期巩膜COLlα2 mRNA表达及其启动子区域CpG岛甲基化水平。方法实验研究。单眼形觉剥夺建立C57BL／6小鼠近视动物模型和恢复期动物模型,分别单眼遮盖4周（48只）和单眼遮盖4周恢复1周（24只）,另外设立正常对照组小鼠36只。实验前后分别用红外偏心摄影验光仪测量小鼠眼球的屈光状态,OCT检测小鼠眼轴长度和玻璃体腔深度。RT—PCR检测巩膜COLlα2 mRNA表达水平;硫化测序聚合酶链式反应（BSP）检测C57BL／6小鼠巩膜COLlα2启动子区域CpG岛甲基化水平。同一小鼠的实验眼和对侧眼比较采用配对t检验,不同组间比较采用独立样本t检验。结果 形觉剥夺4周,实验眼相比对侧眼形成明显的相对近视（t=-2.64,P〈0．05）,并伴有眼轴和玻璃体腔延长。形觉剥夺4周恢复1周后,相对近视和延长的眼轴和玻璃体腔长度都获得恢复。形觉剥夺4周后,实验眼和正常对照眼相比COLlcα2mRNA表达明显下降（t=3．05,P〈0．05）,形觉剥夺4周恢复1周实验眼与正常对照眼相比差异无统计学意义。形觉剥夺4周,实验眼和对侧眼及正常对照眼COLlα2启动子区域CpG岛甲基化水平差异均无统计学意义。结论小鼠单眼形觉剥夺4周可诱导出相对近视,巩膜内COLlα2 mRNA表达明显下降,但该改变与其基因启动子区CpG岛的甲基化状态无关．     

形觉剥夺性眼病与轴性近视关系的探讨

目的　研究形觉剥夺对眼球发育及屈光状态的影响 ,探讨近视眼发病机理及近视发生的危险因素。方法　对一组单眼患早期形觉剥夺性眼病患者的眼球各屈光因子 ,进行生物学测量比较 ,确定其屈光状态 ,并用t检验及多元相关分析的方法找出形觉剥夺性近视的危害因子。结果　患眼与健眼相比 ,患眼有较明显的近视倾向 ,平均屈光力相差 1 2 0 1D。两组比较角膜屈光力、晶状体厚度差异无显著性意义 ;前房深度、玻璃体腔长度、眼轴长度、眼的屈光状态差异均具有显著性意义。玻璃体腔长度为近视眼发生的主要危险因素。结论　早期形觉剥夺可发生近视眼 ,其主要危险因子是眼轴长度 ,主要危害部位在眼后段。尽早去除形觉剥夺 ,保持或恢复视觉发育敏感期的正常视觉环境 ,有利于预防近视眼的发生。     

Effects of optical defocus and spatial contrast on anterior chamber depth in chicks

The goal of this study was to investigate the effect of optical defocus and spatial contrast on refractive development and, in particular,on anterior chamber growth. Ninety chicks were raised from day 4-10 post-hatching wearing monocular lenses (+/-10 Dor 0 D), in an environment with either high, low or no spatial contrast patterns: 30%, 6% or 0% contrast, respectively. At day 10, the chicks' refractive state and ocular components were assessed using retinoscopy and A-scan ultrasonography. Ocular defocus resulted in sign-dependent significant differences in refractive error, axial length and vitreous chamber depth. Lens wear also led to significant spatial contrast dependent changes in anterior chamber depth. Varying ambient spatial contrast in the chick's environment did not inhibit emmetropization processes; however, anterior chamber growth was particularly susceptible to changes in spatial contrast.     

哌仑西平影响豚鼠实验性近视眼的研究

目的 探讨玻璃体腔注射选择性M_1受体拮抗剂哌仑西平对豚鼠形觉剥夺性近视眼视网膜、脉络膜、巩膜和虹膜-睫状体组织中M_1和M_4受体mRNA表达的影响.方法 采用随机分组设计的实验研究.1～2周龄的三色豚鼠24只,随机分为4组:正常对照组(N)6只,单纯形觉剥夺组(FDM)6只,药物对照组(S)6只,哌仑西平组(P)6只,均以左眼为实验眼,P组隔日玻璃体腔注射500μg哌仑西平;S组隔日玻璃体腔注射生理盐水.21 d后结束实验.提取各组眼视网膜、脉络膜、巩膜和虹膜-睫状体组织总RNA,半定量RT-PCR检测M_1和M_4亚型mRNA表达变化.3组间数据的比较采用单因素方差分析和Tukey post hoc检验.结果 21d时,FDM与N组相比较,FDM组眼轴相对延长0.29mm,产生相对近视-4.92 D,差异有统计学意义(P<0.001).P组与S组相比较,眼轴相对减少了0.30 mm,产生+0.88 D的相对远视,差异均有统计学意义(P<0.001).S组与FDM之间屈光度数的差异无统计学意义;而眼轴变化有统计学意义(S组相对延长0.08 mm,而FDM组相对延长0.29/mm).半定量PCR结果显示:P组与S组相比较,其视网膜、脉络膜和虹膜睫状体组织M_1和M_4亚型mRNA的表达差异无统计学意义(P>0.05).而在后极部巩膜组织,M_1和M_4亚型mRNA的表达较药物对照组显著性增加(P<0.05),其中M_1受体表达增加19.16%,M_4受体表达增加64.29%.结论 哌仑西平能够有效抑制豚鼠形觉剥夺近视的发展.巩膜组织M_1和M_4亚型及其胆碱能通路可能参与M受体拮抗剂抑制近视发展.     

Effects of brief periods of unrestricted vision on the development of form-deprivation myopia in monkeys

PURPOSE: To characterize the temporal integration properties of the mechanisms responsible for form-deprivation myopia (FDM), the effects of brief daily periods of unrestricted vision on the degree of FDM were investigated in infant monkeys. METHODS: Starting at approximately 3 weeks of age, unilateral form deprivation was produced in 24 infant rhesus monkeys by securing a diffuser spectacle lens in front of one eye and a clear, zero-powered lens in front of the fellow eye. During the treatment period (17 +/- 2 weeks), six infants wore the diffuser lenses continuously. In the other experimental infants, the diffuser lenses were removed each day and replaced with clear, zero-powered lenses for 1 (n = 7), 2 (n = 7), or 4 hours (n = 4). Refractive development was assessed by retinoscopy and A-scan ultrasonography. Control data were obtained from 11 normal infants and 3 infants reared with zero-powered lenses over both eyes. RESULTS: The degree of FDM varied significantly with the duration of unrestricted vision. Continuous form deprivation produced -5.2 +/- 3.6 D of relative axial myopia. However, 1 hour of unrestricted vision was sufficient to reduce the degree of axial FDM by more than 50% (-1.7 +/- 3.2 D). The infants that were allowed 4 hours of unrestricted vision exhibited only -0.4 +/- 0.5 D of FDM. CONCLUSIONS: As observed in chickens and tree shrews, relatively long periods of form deprivation can be counterbalanced by quite short periods of unrestricted vision. These results indicate that the processes or signals that promote axial elongation in monkeys are comparatively weak or easily overridden by factors that slow ocular growth.     

The postnatal development of the oscillatory potentials of the electroretinogram. I. Basic characteristics

The postnatal development of the oscillatory potentials (OPs) of the rat electroretinogram (ERG) was studied. The appearance and/or completion of the development of the individual oscillatory peaks differed from that of the a- and b-waves as well as from each other. The OPs appeared postnatally one to two days later than the a- and b-waves, respectively. The first oscillatory peak, O1, was present before the second, O2, which appeared before the later wavelets, O3, O4 and O5. The pattern of maturation of the oscillatory peaks in relatively more scotopic conditions differed from that in relatively more photopic ones. The summed amplitudes of the OPs attained adult size earlier (about two weeks) during relatively more scotopic conditions. The peak time of each oscillation gradually decreased with age. These findings show that the origin of the OPs is different from that of the a- and b-waves of the ERG and strongly indicate different origins of the earlier OPs from the later ones. Thirdly, the scotopic mechanism underlying the OPs seems to mature faster than the photopic system involved in the generation of the OPs.     

Retinal dysfunction in diabetic ren-2 rats is ameliorated by treatment with valsartan but not atenolol

PURPOSE: To determine whether diabetes leads to retinal neuronal dysfunction in hypertensive transgenic (mRen-2)27 rats (Ren-2), and whether the effect can be prevented by treatment of hypertension with either the angiotensin-1 receptor blocker (AT1-RB) valsartan or the beta1-adrenergic receptor antagonist atenolol. METHODS: Six-week-old Ren-2 rats were made diabetic (streptozotocin 55 mg/kg; n = 34) or remained nondiabetic (0.1 M citrate buffer; n = 43) and studied for 20 weeks. A subset of animals received valsartan (4 mg/kg per day) or atenolol (30 mg/kg per day) by gavage. Sprague-Dawley (SD) rats served as normotensive controls for blood pressure (BP). We evaluated retinal function in all groups with a paired-flash electroretinogram over high light intensities (0.5-2.0 log cd-s . m(-2)), to isolate rod and cone responses. RESULTS: A reduction in amplitude of all electroretinogram components (PIII, PII, OPs, cone PII) was found in nondiabetic Ren-2 compared with nondiabetic SD rats. A further reduction was observed in diabetic Ren-2 rats. Treatment of both nondiabetic and diabetic Ren-2 rats with valsartan or atenolol reduced BP to within normal limits. This reduction produced some improvement in function in treated nondiabetic Ren-2 rats. However, in treated diabetic Ren-2 rats, retinal dysfunction was ameliorated by valsartan but not by atenolol, with a significant improvement (P < 0.05) observed in all components of the electroretinogram, with the exception of the OPs. CONCLUSIONS: These findings suggest that hypertension induces retinal dysfunction that is exacerbated with diabetes and ameliorated by treatment with an AT1-RB, and not just by normalizing BP. These data provide further evidence for the importance of the renin-angiotensin system in development of diabetic complications.     

低压缺氧对LASIK术后视功能的影响

目的观察LASIK术后人群在低压缺氧环境中视功能变化情况,了解准分子激光角膜屈光手术眼在飞行特殊环境的适应性。方法自身前后对照研究。20名（40眼）健康志愿者,平均年龄为（23.8±1.2）岁,准分子激光近视矫正术后1年。低压舱上升前测量眼压、近立体视、色觉、屈光度、对比敏感度（双眼明视、暗视眩光下空间频率3、6、12、18 c/d的对比敏感度值）,低压舱以30 m/s速度上升至5 000 m高度,在此高度停留10 min后再次测量,此过程无供氧,测量后低压舱以10～15 m/s速度下降至地面。对相应数据采用配对t检验进行分析。结果低压舱实验前后眼压未见明显变化[（右眼（13.0±1.7）mmHgvs. （13.0±2.1）mmHg,t=-0.56,P>0.05;左眼（13.0±2.0 mmHg vs. （13.0±2.0）mmHg,t=-0.81,P>0.05）];近立体视[（21.5±2.4）弧秒 vs. （27.6±8.3）弧秒,t=-3.39,P<0.05）及色觉（9.60±2.73 vs. 27.20±8.57,t=-2.81,P<0.05）]下降;等效球镜度[（右眼（-0.90±0.61）D vs. （-1.08±0.75）D,t=1.71,P>0.05,左眼（-1.21±0.61）D vs. （-1.06±0.54）D,t=-1.33,P>0.05）差异无统计学意义;对比敏感度（18 c/d暗视眩光环境对比敏感度降低P<0.05,其他情况均未见降低）。结论低压缺氧环境对准分子激光术后远期人群的眼压、屈光度、对比敏感度（除高频暗视眩光）均无影响;近立体视、色觉及高频暗视眩光条件的对比敏感度下降。     

The postnatal development of the oscillatory potentials of the electroretinogram. III. Scotopic characteristics.

The postnatal development of the oscillatory potentials (OPs) of the rat electroretinogram (ERG) was studied during more extreme scotopic conditions. Enhancement of scotopic conditions did not facilitate any earlier appearance of the OPs, including the later ones, compared to previously studied less scotopic conditions. The oscillatory activity appeared at Days 12 to 15, and increased rapidly up to Day 17, which coincided with the major period of development of the photoreceptors. After the physiological opening of the eyelids there was a decline of the OPs. We propose that the decline of the oscillatory activity induced during more extreme scotopic conditions is related to early cell death in the distal retina and/or to developmental neuronal plasticity in the proximal retina.     

Retinal Dopamine D2 Receptors Participate in the Development of Myopia in Mice

PurposeTo learn more about the locations of dopamine D2 receptors (D2Rs) that regulate form-deprivation myopia (FDM), using different transgenic mouse models.MethodsOne eye of D2R-knockout (KO) mice and wild-type littermates was subjected to four weeks of monocular FDM, whereas the fellow eye served as control. Mice in both groups received daily intraperitoneal injections of either the D2R antagonist sulpiride (8 µg/g) or vehicle alone. FDM was also induced in retina- (Six3^creD2R^fl/fl) or fibroblast-specific (S100a4^creD2R^fl/fl) D2R-KO mice. A subset of retina-specific D2R-KO mice and D2R^fl/fl littermates were also given sulpiride or vehicle injections. Refraction was measured with an eccentric infrared photorefractor, and other biometric parameters were measured by optical coherence tomography (n ≈ 20 for each group).ResultsFDM development was attenuated in wild-type littermates treated with sulpiride. However, this inhibitory effect disappeared in the D2R-KO mice, suggesting that antagonizing D2Rs suppressed myopia development. Similarly, the development of myopia was partially inhibited by retina-specific (deletion efficiency: 94.7%) but not fibroblast-specific (66.9%) D2R-KO. The sulpiride-mediated inhibitory effects on FDM also disappeared with retinal D2R-KO, suggesting that antagonizing D2Rs outside the retina may not attenuate myopia. Changes in axial length were less marked than changes in refraction, but in general the two were correlated.ConclusionsThis study demonstrates that D2Rs located in the retina participate in dopaminergic regulation of FDM in mice. These findings provide an important and fundamental basis for further exploring the retinal mechanism(s) involved in dopamine signaling and myopia development.     

Ambient Light Regulates Retinal Dopamine Signaling and Myopia Susceptibility

PurposeExposure to high-intensity or outdoor lighting has been shown to decrease the severity of myopia in both human epidemiological studies and animal models. Currently, it is not fully understood how light interacts with visual signaling to impact myopia. Previous work performed in the mouse retina has demonstrated that functional rod photoreceptors are needed to develop experimentally-induced myopia, alluding to an essential role for rod signaling in refractive development.MethodsTo determine whether dim rod-dominated illuminance levels influence myopia susceptibility, we housed male C57BL/6J mice under 12:12 light/dark cycles with scotopic (1.6 × 10⁻³ candela/m²), mesopic (1.6 × 10¹ cd/m²), or photopic (4.7 × 10³ cd/m²) lighting from post-natal day 23 (P23) to P38. Half the mice received monocular exposure to −10 diopter (D) lens defocus from P28–38. Molecular assays to measure expression and content of DA-related genes and protein were conducted to determine how illuminance and lens defocus alter dopamine (DA) synthesis, storage, uptake, and degradation and affect myopia susceptibility in mice.ResultsWe found that mice exposed to either scotopic or photopic lighting developed significantly less severe myopic refractive shifts (lens treated eye minus contralateral eye; –1.62 ± 0.37D and −1.74 ± 0.44D, respectively) than mice exposed to mesopic lighting (–3.61 ± 0.50D; P < 0.005). The 3,4-dihydroxyphenylacetic acid /DA ratio, indicating DA activity, was highest under photopic light regardless of lens defocus treatment (controls: 0.09 ± 0.011 pg/mg, lens defocus: 0.08 ± 0.008 pg/mg).ConclusionsLens defocus interacted with ambient conditions to differentially alter myopia susceptibility and DA-related genes and proteins. Collectively, these results show that scotopic and photopic lighting protect against lens-induced myopia, potentially indicating that a broad range of light levels are important in refractive development.