De Bremaeker N, Dewael Y, Baguet F, Mallefet J
Laboratory of Animal Physiology, Université Catholique de Louvain, Place Croix du Sud, 5, B-1348 Louvain-la-Neuve, Belgium.
Luminescence. 2000 May-Jun;15(3):159-63. doi: 10.1002/1522-7243(200005/06)15:3<159::AID-BIO581>3.0.CO;2-P.
We investigated the effects of cyclic nucleotides (cGMP, cAMP) and the phosphoinositide IP(3) on the luminescence of the ophiuroid Amphipholis squamata. The cGMP analogue, dibutyryl-cGMP, and the guanylate cyclase activator, sodium nitroprusside, had no effect on the luminescence. The cAMP analogue, dibutyryl-cAMP, and the adenylate cyclase activator, forskolin, triggered luminescence. Moreover, the adenylate cyclase inhibitor, MDL-12330A, significantly reduced ACh-induced luminescence. The phospholipase C inhibitor, U-73122, also significantly reduced ACh-induced luminescence. The results suggest that ACh-induced luminescence is mediated by both cAMP and IP(3) pathways but not by cGMP. The effects of calcium-free ASW confirmed this hypothesis. A hypothetical scheme of the transduction mechanisms involved in the intracellular control of luminescence is presented.
我们研究了环核苷酸(cGMP、cAMP)和磷酸肌醇IP(3)对蛇尾纲动物鳞蛇尾发光的影响。cGMP类似物二丁酰-cGMP和鸟苷酸环化酶激活剂硝普钠对发光没有影响。cAMP类似物二丁酰-cAMP和腺苷酸环化酶激活剂福斯可林引发了发光。此外,腺苷酸环化酶抑制剂MDL-12330A显著降低了乙酰胆碱诱导的发光。磷脂酶C抑制剂U-73122也显著降低了乙酰胆碱诱导的发光。结果表明,乙酰胆碱诱导的发光是由cAMP和IP(3)途径介导的,而不是由cGMP介导的。无钙人工海水的作用证实了这一假设。本文提出了一个参与发光细胞内控制的转导机制的假设方案。