玻璃体内注射多巴胺d2样(和D4)受体激动剂,而不是d1样受体激动剂,可以减少树鼩的形式剥夺性近视。

IF 1.1 4区 医学 Q4 NEUROSCIENCES
Alexander H Ward, John T Siegwart, Michael R Frost, Thomas T Norton
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引用次数: 24

摘要

我们研究了玻璃体内注射d1样和d2样多巴胺受体激动剂和拮抗剂以及D4受体药物对树鼩(与灵长类密切相关的哺乳动物)形式剥夺性近视(FDM)的影响。在11个组(每组n = 7)中,我们在11天的治疗期间测量了单眼形态剥夺(FD)产生的FDM量。未治疗的同伴眼作为对照。动物也在FD眼每天接受5µL玻璃体内注射。对照组给予0.85% NaCl溶液。四组接受更高或更低剂量的d1样受体激动剂(SKF38393)或拮抗剂(SCH23390)。四组分别接受或高或低剂量的d2样受体激动剂(喹匹罗)或拮抗剂(spiperone)。两组均给予D4受体激动剂(PD168077)或拮抗剂(PD168568)。每天测量折光;在第1天(治疗前)和第12天测量轴向分量尺寸。我们发现,在接受d1样受体激动剂或拮抗剂的组中,FDM的发展和眼部成分尺寸的改变与NaCl组没有差异。与NaCl组相比,接受高剂量d2样受体激动剂或拮抗剂的组FDM明显减少,玻璃体腔明显缩短。D4受体激动剂,而不是拮抗剂,在减少FDM方面几乎与d2样激动剂一样有效。因此,使用玻璃体内给药,我们没有发现证据支持d1样受体途径在树鼩中减少FDM的作用。多巴胺d2样激动剂对FDM的减少支持了d2样受体途径在FDM控制中的作用。D4受体激动剂而非D4拮抗剂能降低FDM,这表明多巴胺D4受体的激活在控制轴向伸长和屈光发育中起重要作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Intravitreally-administered dopamine D2-like (and D4), but not D1-like, receptor agonists reduce form-deprivation myopia in tree shrews.

Intravitreally-administered dopamine D2-like (and D4), but not D1-like, receptor agonists reduce form-deprivation myopia in tree shrews.

Intravitreally-administered dopamine D2-like (and D4), but not D1-like, receptor agonists reduce form-deprivation myopia in tree shrews.

We examined the effect of intravitreal injections of D1-like and D2-like dopamine receptor agonists and antagonists and D4 receptor drugs on form-deprivation myopia (FDM) in tree shrews, mammals closely related to primates. In eleven groups (n = 7 per group), we measured the amount of FDM produced by monocular form deprivation (FD) over an 11-day treatment period. The untreated fellow eye served as a control. Animals also received daily 5 µL intravitreal injections in the FD eye. The reference group received 0.85% NaCl vehicle. Four groups received a higher, or lower, dose of a D1-like receptor agonist (SKF38393) or antagonist (SCH23390). Four groups received a higher, or lower, dose of a D2-like receptor agonist (quinpirole) or antagonist (spiperone). Two groups received the D4 receptor agonist (PD168077) or antagonist (PD168568). Refractions were measured daily; axial component dimensions were measured on day 1 (before treatment) and day 12. We found that in groups receiving the D1-like receptor agonist or antagonist, the development of FDM and altered ocular component dimensions did not differ from the NaCl group. Groups receiving the D2-like receptor agonist or antagonist at the higher dose developed significantly less FDM and had shorter vitreous chambers than the NaCl group. The D4 receptor agonist, but not the antagonist, was nearly as effective as the D2-like agonist in reducing FDM. Thus, using intravitreally-administered agents, we did not find evidence supporting a role for the D1-like receptor pathway in reducing FDM in tree shrews. The reduction of FDM by the dopamine D2-like agonist supported a role for the D2-like receptor pathway in the control of FDM. The reduction of FDM by the D4 receptor agonist, but not the D4 antagonist, suggests an important role for activation of the dopamine D4 receptor in the control of axial elongation and refractive development.

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来源期刊
Visual Neuroscience
Visual Neuroscience 医学-神经科学
CiteScore
2.20
自引率
5.30%
发文量
8
审稿时长
>12 weeks
期刊介绍: Visual Neuroscience is an international journal devoted to the publication of experimental and theoretical research on biological mechanisms of vision. A major goal of publication is to bring together in one journal a broad range of studies that reflect the diversity and originality of all aspects of neuroscience research relating to the visual system. Contributions may address molecular, cellular or systems-level processes in either vertebrate or invertebrate species. The journal publishes work based on a wide range of technical approaches, including molecular genetics, anatomy, physiology, psychophysics and imaging, and utilizing comparative, developmental, theoretical or computational approaches to understand the biology of vision and visuo-motor control. The journal also publishes research seeking to understand disorders of the visual system and strategies for restoring vision. Studies based exclusively on clinical, psychophysiological or behavioral data are welcomed, provided that they address questions concerning neural mechanisms of vision or provide insight into visual dysfunction.
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