Rubin L J, Nolte J F
Nature. 1984;307(5951):551-3. doi: 10.1038/307551a0.
The light-induced constriction of the irises of some vertebrates is mediated by photosensitive pupillary sphincter cells, which have rhodopsin molecules in their sarcolemmas. Light-induced isomerization of these rhodopsin molecules leads to the release of Ca2+ from an internal pool, which in turn activate the contractile proteins. A central nervous reflex is therefore not essential for the light responsiveness of these irises, but they do appear to be innervated. The photosensitive iris of the toad receives sympathetic (adrenergic) innervation. Stimulation of sympathetic nerves to the eye or application of adrenergic agonists to the iris cause pupillary dilation due to relaxation of the sphincter muscle. We show here that beta-adrenergic stimulation of toad sphincter cells modulates their photoresponses by elevating the intracellular levels of cyclic AMP. However, cyclic AMP does not appear to be involved in the transduction event but rather alters the availability of Ca2+ for contraction.
一些脊椎动物虹膜的光诱导收缩是由光敏瞳孔括约肌细胞介导的，这些细胞的肌膜中有视紫红质分子。这些视紫红质分子的光诱导异构化导致Ca2+从内部储存库释放，进而激活收缩蛋白。因此，中枢神经反射对于这些虹膜的光反应性并非必不可少，但它们似乎确实接受神经支配。蟾蜍的光敏虹膜接受交感（肾上腺素能）神经支配。刺激眼部的交感神经或向虹膜应用肾上腺素能激动剂会导致瞳孔扩张，这是由于括约肌肌肉松弛所致。我们在此表明，蟾蜍括约肌细胞的β-肾上腺素能刺激通过提高细胞内环磷酸腺苷（cAMP）水平来调节其光反应。然而，cAMP似乎并不参与转导事件，而是改变了用于收缩的Ca2+的可用性。
