Evidence for a potential role of glucagon during eye growth regulation in chicks

Evidence for a potential role of glucagon during eye growth regulation in chicks
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DOI:
10.1017/s0952523802196064
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发表时间:
2002-11-01
影响因子:
1.9
通讯作者:
Schaeffel, F
Schaeffel, F
中科院分区:
医学4区
文献类型:
--
作者:
Feldkaemper, MP;Schaeffel, F

文献摘要

被引文献

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眼睛的生长和折射是由视网膜的视觉处理来调节的。到目前为止,视网膜释放的诱导这些变化的信使在很大程度上是未知的。以前,人们发现胰高血糖素无分泌细胞对视网膜图像中的散焦甚至其迹象有反应。直接早期基因产物ZENK的表达在带正晶状体的雏鸡中增加,在带负晶状体的雏鸡中减少。此外,在阳性晶状体治疗期间,视网膜胰高血糖素mRNA的数量增加。因此,这些细胞似乎对眼睛生长的视觉调节有贡献,而胰高血糖素可能作为眼睛生长的停止信号。本研究的目的是为胰高血糖素在眼睛生长的视觉控制中的作用积累进一步的证据。分别注射不同剂量的胰高血糖素拮抗剂des-His(1)-Glu(9)-胰高血糖素酰胺或激动剂Lys(17)、Glu(18)、Glu(21)-胰高血糖素后,给予正透镜和负透镜。分别用自动红外光折射仪和a超扫描仪记录屈光发育和眼球生长情况。胰高血糖素拮抗剂抑制远视的发展,虽然浓度范围很窄,最多抑制50%,但不抑制近视的发展。相比之下,激动剂以剂量依赖的方式抑制近视的发展。高浓度时,它还能预防远视的发展。采用放射免疫法测定晶状体处理雏鸡视网膜和脉络膜中胰高血糖素肽的含量及其日变化。负晶状体治疗后视网膜胰高血糖素含量降低,正晶状体治疗后脉络膜胰高血糖素含量升高。视网膜胰高血糖素含量无昼夜变化。此外,采用光动力学眼震模式,研究了胰高血糖素和拮抗剂des-His(1)-Glu(9)-胰高血糖素-酰胺对阈上对比敏感性的影响。胰高血糖素降低了对比敏感性(这可能与生长抑制信号有关),而拮抗剂des-His(1)-Glu(9)-胰高血糖素-酰胺增加了对比敏感性。研究结果与胰高血糖素在小鸡眼睛生长的视觉控制中起作用的假设一致。
Eye growth and refraction are regulated by visual processing in the retina. Until now, the messengers released by the retina to induce these changes are largely unknown. Previously, it was found that glucagon amacrine cells respond to defocus in the retinal image and even to its sign. The expression of the immediate-early gene product ZENK increased in this cell population in eyes wearing plus lenses and decreased in minus lens-treated chicks. Moreover, it was shown that the amount of retinal glucagon mRNA increased during treatment with positive lenses. Therefore, it seems likely that these cells contribute to the visual regulation of ocular growth and that glucagon may act as a stop signal for eye growth. The purpose of the present study was to accumulate further evidence for a role of glucagon in the visual control of eye growth. Chicks were treated with plus and minus lenses after injection of different amounts of the glucagon antagonist des-His(1)-Glu(9)-glucagon-amide or the agonist Lys(17),(18),Glu(21)-glucagon, respectively. Refractive development and eye growth were recorded by automated infrared photorefraction and A-scan ultrasound, respectively. The glucagon antagonist inhibited hyperopia development, albeit only in a narrow concentration range, and at most by 50%, but not myopia development. In contrast, the agonist inhibited myopia development in a dose-dependent fashion. At high concentrations, it also prevented hyperopia development. The amount of glucagon peptide in the retinae and choroids of lens-treated chicks and its diurnal variation was measured by using a radio-immunoassay. Retinal glucagon content decreased after minus lens treatment and choroidal glucagon content increased after plus lens treatment. No diurnal variation in the retinal amount of glucagon was detected. In addition, using an optokinetic nystagmus paradigm, the effect of glucagon and the antagonist des-His(1)-Glu(9)-glucagon-amide on suprathreshold contrast sensitivity was studied. Glucagon reduced contrast sensitivity (which might be linked to a signal for growth inhibition) whereas the antagonist des-His(1)-Glu(9)-glucagon-amide increased contrast sensitivity. The results of the study are in line with the hypothesis that glucagon plays a role in the visual control of eye growth in the chick.