Cholinergic amacrine cells are not required for the progression and atropine-mediated suppression of form-deprivation myopia
Cholinergic amacrine cells are not required for the progression and atropine-mediated suppression of form-deprivation myopia
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DOI：
10.1016/s0006-8993(98)00188-7
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发表时间：
1998-05-25
期刊：
影响因子：
2.9
通讯作者：
Stell, WK
中科院分区：
文献类型：
--
作者：
Fischer, AJ;Miethke, P;Stell, WK
毒蕈碱胆碱能途径与眼生长的视觉控制有关。然而，乙酰胆碱的来源和通过毒蕈碱乙酰胆碱受体（mAChR）调节眼生长的组织仍然未知。我们试图确定是否视网膜来源的乙酰胆碱和mAChRs有助于视觉引导的眼睛生长的小鸡。通过眼内注射乙基胆碱氮芥氮丙啶离子（ECMA;一种选择性胆碱毒素）或使君子酸（QA;一种破坏许多无长突细胞（包括释放乙酰胆碱的细胞）的兴奋性毒素）来消融胆碱能无长突细胞。胆碱能途径的中断进行了评估，免疫细胞化学抗体的乙酰胆碱合成酶胆碱乙酰转移酶（ChAT）和三种不同的亚型的mAChR，并通过生化测定ChAT活性。ECMA（25 nmol）破坏了胆碱能无长突细胞的四种亚型中的两种，并减弱了视网膜ChAT活性，但留下了完整的视网膜mAChR免疫反应。QA（200 nmol）破坏了所有四种亚型胆碱能无长突细胞的大部分，并消除了视网膜中大部分mAChR免疫反应性和ChAT活性。ECMA和QA对脉络膜中的mAChRs或胆碱能纤维没有明显影响，仅略微降低脉络膜ChAT活性，并且对眼前段中的ChAT活性几乎没有影响。毒素处理的眼睛保持正视，并通过过度生长和近视来应对形觉剥夺。此外，每天玻璃体内注射40微克阿托品6天到形觉剥夺毒素治疗的眼睛完全防止眼球伸长和近视。我们的结论是，无论是胆碱能无长突细胞，也不需要在视网膜mAChRs的眼睛生长的视觉调节，阿托品可能发挥其生长抑制作用的影响，作用于视网膜外mAChRs，可能在脉络膜，视网膜色素上皮细胞，或巩膜。(C)1998 Elsevier Science B. V.保留所有权利。
Muscarinic cholinergic pathways have been implicated in the visual control of ocular growth. However, the source(s) of acetylcholine and the tissue(s) which regulate ocular growth via muscarinic acetylcholine receptors (mAChRs) remain unknown. We sought to determine whether retinal sources of acetylcholine and mAChRs contribute to visually guided ocular growth in the chick. Cholinergic amacrine cells were ablated by intraocular injections of either ethylcholine mustard aziridinium ion (ECMA; a selective cholinotoxin) or quisqualic acid (QA; an excitotoxin that destroys many amacrine cells, including those that release acetylcholine). Disruption of cholinergic pathways was assessed immunocytochemically with antibodies to the acetylcholine-synthesizing enzyme choline acetyltransferase (ChAT) and three different isoforms of mAChR, and by biochemical assay for ChAT activity. ECMA (25 nmol) destroyed two of the four subtypes of cholinergic amacrine cells and attenuated retinal ChAT activity, but left retinal mAChR-immunoreactivity intact. QA (200 nmol) destroyed the majority of all four subtypes of cholinergic amacrine cells, and ablated most mAChR-immunoreactivity and ChAT activity in the retina. ECMA and QA had no apparent effect on mAChRs or cholinergic fibres in the choroid, only marginally reduced choroidal ChAT activity, and had little effect on ChAT activity in the anterior segment. Toxin-treated eyes remained emmetropic and responded to form-deprivation by growing excessively and becoming myopic. Furthermore, daily intravitreal injection of 40 mu g atropine for 6 days into form-deprived toxin-treated eyes completely prevented ocular elongation and myopia. We conclude that neither cholinergic amacrine cells nor mAChRs in the retina are required for visual regulation of ocular growth, and that atropine may exert its growth-suppressing influence by acting upon extraretinal mAChRs, possibly in the choroid, retinal pigmented epithelium, or sclera. (C) 1998 Elsevier Science B.V. All rights reserved.