Anctil M, Case J F
Cell Tissue Res. 1976 Feb 25;166(3):365-88. doi: 10.1007/BF00220132.
The effects of 6-hydroxydopamine (6-OHDA) on the bioluminescent response of Porichthys photophores were investigated as part of a pharmacological study of the neural control of luminescence in this fish. Subcutaneous injections of 6-OHDA induce a luminescent response similar to that of norepinephrine (NE), suggesting a sympathomimetic action. The luminescent response to electrical stimulation is almost completely and irreversibly abolished within 24 hours following low-dose treatment of the photophores with 6-OHDA, while the sensitivity of these organs to exogenous NE is increased significantly over the few days post-treatment. During this period the photophores continously emitted a steady low-level glow. Electronmicroscopic studies of such photophores revealed progressive destruction of the nerve endings. Photophore luminescent sensitivty to NE subsequently became sub-normal, and at this stage electron microscopy revealed an increasingly larger number of damaged photocytes, supportive cells and, in one case, lens cells. From these results it is suggested that 6-OHDA initially impairs neuro-photocyte transmission by destroying catecholaminergic nerve endings. In turn, the transmitter reuptake mechanism is also impaired, thus accounting for development of supersensitive responses to exogenous NE. Subnormal luminescent responses to NE appear as a result of loss of photocyte competence due to structural deterioration. The latter are interpreted as the consequence of removal of trophic factors supplied by the photophore adrenergic innervation. Suppression of luminescent response to both electrical stimulation and exogenous NE in photophores treated with higher doses of 6-OHDA, may be due to a direct effect of this drug on the receptor sites of the photocytes.
作为对这种鱼类发光神经控制的药理学研究的一部分,研究了6-羟基多巴胺(6-OHDA)对多锯鲈发光器生物发光反应的影响。皮下注射6-OHDA会引发类似于去甲肾上腺素(NE)的发光反应,表明具有拟交感神经作用。在用6-OHDA对发光器进行低剂量处理后的24小时内,对电刺激的发光反应几乎完全且不可逆地被消除,而在处理后的几天里,这些器官对外源性NE的敏感性显著增加。在此期间,发光器持续发出稳定的低水平光。对这种发光器的电子显微镜研究显示神经末梢逐渐遭到破坏。发光器对NE的发光敏感性随后变得低于正常水平,在此阶段电子显微镜显示受损的发光细胞、支持细胞数量越来越多,在一个案例中还包括晶状体细胞。从这些结果表明,6-OHDA最初通过破坏儿茶酚胺能神经末梢损害神经-发光细胞传递。反过来,递质再摄取机制也受到损害,从而解释了对外源性NE超敏反应的发展。对NE的发光反应低于正常水平是由于发光细胞因结构恶化而丧失功能所致。后者被解释为发光器肾上腺素能神经支配提供的营养因子被去除的结果。用更高剂量的6-OHDA处理的发光器对电刺激和外源性NE的发光反应受到抑制,可能是由于这种药物对发光细胞受体部位的直接作用。