Suzuki Y, Nakano T, Sears M
Department of Ophthalmology and Visual Science, Yale University School of Medicine, New Haven, CT 06520-8061, USA.
Curr Eye Res. 1997 Feb;16(2):166-75. doi: 10.1076/ceyr.16.2.166.5095.
We investigated patterns of evoked calcium signals to learn about the function of the calcium second messenger system in ciliary epithelium.
Isolated infact ciliary processes were loaded with fluo-3/AM and observed with a Bio-Rad MRC-600 laser scanning confocal imaging system, before, during, and after perfusion with catecholamines, cholinergic agents, and autocoids.
One microM acetylcholine (ACH) and 10 microM carbachol (CARB) induced an atropine-sensitive increase in intracellular free calcium ion concentration ([Ca2+]i), considerably greater in NPE than in PE. 10 microM epinephrine (EPI) and 100 microM phenylephrine (PHE) increased [Ca2+]i in NPE and PE, in this case PE > NPE. These effects were blocked by prazosin. 10 mM caffeine (CAF) increased of [Ca2+]i in NPE and PE (NPE > PE) and sometimes produced very slow oscillations with an interval of 10 to 25 s. Prior administration of CAF strongly suppressed the effects of ACH, CARB, EPI, PHE, histamine, and adenosine 5-triphosphate (ATP). One hundred microM ryanodine (RYA) or thapsigargin (TG) increased [Ca2+]i in NPE and PE (NPE > PE).
In the ciliary epithelium: (1) different patterns of evoked transients and oscillations of calcium were seen in response to agonists; (2) NPE appeared to contain a predominance of muscarinic receptors, while the PE is dominated by alpha 1-adrenergic receptors and (3) the increase in [Ca2+]i by CAF or RYA or TG in either cell layer and the blocking effects of these agents upon agonist, evoking increases in [Ca2+]i, suggested involvement of both the cyclic adenosine diphosphate ribose and the inositol 1, 4, 5 triphosphate (InsP3) systems in the regulation of intracellular calcium.
我们研究诱发钙信号模式，以了解钙第二信使系统在睫状体上皮中的功能。
将分离的完整睫状突用氟-3/AM加载，并在灌注儿茶酚胺、胆碱能药物和自分泌物质之前、期间和之后，用Bio-Rad MRC-600激光扫描共聚焦成像系统进行观察。
1微摩尔乙酰胆碱（ACH）和10微摩尔卡巴胆碱（CARB）可诱导细胞内游离钙离子浓度（[Ca2+]i）出现阿托品敏感的升高，非色素上皮（NPE）中的升高幅度明显大于色素上皮（PE）。10微摩尔肾上腺素（EPI）和100微摩尔去氧肾上腺素（PHE）可使NPE和PE中的[Ca2+]i升高，在这种情况下，PE>NPE。这些作用可被哌唑嗪阻断。10毫摩尔咖啡因（CAF）可使NPE和PE中的[Ca2+]i升高（NPE>PE），有时会产生间隔为10至25秒的非常缓慢的振荡。预先给予CAF可强烈抑制ACH、CARB、EPI、PHE、组胺和三磷酸腺苷（ATP）的作用。100微摩尔ryanodine（RYA）或毒胡萝卜素（TG）可使NPE和PE中的[Ca2+]i升高（NPE>PE）。
在睫状体上皮中：（1）对激动剂的反应中可见不同模式的诱发钙瞬变和振荡；（2）NPE似乎主要含有毒蕈碱受体，而PE则以α1-肾上腺素能受体为主；（3）CAF、RYA或TG在任一细胞层中使[Ca2+]i升高以及这些药物对激动剂诱发[Ca2+]i升高的阻断作用，提示环磷酸腺苷二磷酸核糖和肌醇1,4,5-三磷酸（InsP3）系统均参与细胞内钙的调节。
