Dearry A, Burnside B
J Neurochem. 1986 Apr;46(4):1022-31. doi: 10.1111/j.1471-4159.1986.tb00613.x.
In the accompanying paper we reported that 3,4-dihydroxyphenylethylamine (dopamine) induced light-adaptive retinomotor movements in teleost photoreceptors and that this effect was mediated by D2 dopamine receptors located on the photoreceptors themselves. In this study, we investigated the effects on cone retinomotor movement of three agents that have been reported by others to modulate retinal dopamine release: gamma-aminobutyric acid (GABA), 5-hydroxytryptamine (5-HT, serotonin), and melatonin. We report here that the GABA antagonists bicuculline and picrotoxin induced light-adaptive cone contraction in dark-adapted green sunfish retinas cultured in constant darkness; thus they mimic the effect of light or exogenously applied dopamine. Since their effects were blocked by either the D2 dopamine antagonist sulpiride or by Co2+, it seems likely that these agents act by enhancing retinal dopamine release. The GABA agonist muscimol produced effects opposite to those of GABA antagonists. Muscimol inhibited light-induced cone contraction in previously dark-adapted retinas and induced dark-adaptive cone elongation in light-adapted retinas. These results suggest that in green sunfish retinas, as has been reported for other retinas, GABA inhibits dopamine release. 5-HT induced light-adaptive cone contraction in dark-adapted retinas; thus 5-HT also mimics the effect of light or exogenously applied dopamine. The effect of 5-HT was blocked by sulpiride, Co2+, or the 5-HT antagonist mianserin. These results suggest that 5-HT induces cone contraction by stimulating dopamine release. Melatonin neither inhibited dopamine-induced cone contraction in retinas cultured in the dark nor induced cone elongation in retinas cultured in the light. Our results suggest that both GABA and 5-HT (but not melatonin) affect cone retinomotor movements in green sunfish by modulating dopamine release: GABA by inhibiting and 5-HT by stimulating dopamine release. We report in the companion paper that dopamine induced contraction in isolated cone fragments. Together these observations strongly suggest that dopamine serves as the final extracellular messenger directly inducing light-adaptive cone retinomotor movement, and that GABA and 5-HT affect these movements by modulating dopamine release.
在随附论文中，我们报道了3,4 - 二羟基苯乙胺（多巴胺）可诱导硬骨鱼光感受器的光适应性视网膜运动，且这种效应是由光感受器自身上的D2多巴胺受体介导的。在本研究中，我们研究了其他研究报道的三种可调节视网膜多巴胺释放的物质对视锥细胞视网膜运动的影响：γ-氨基丁酸（GABA）、5 - 羟色胺（5 - HT，血清素）和褪黑素。我们在此报告，GABA拮抗剂荷包牡丹碱和印防己毒素可在持续黑暗中培养的暗适应绿太阳鱼视网膜中诱导光适应性视锥细胞收缩；因此它们模拟了光或外源性应用多巴胺的作用。由于它们的作用可被D2多巴胺拮抗剂舒必利或Co2 +阻断，这些物质似乎很可能是通过增强视网膜多巴胺释放来发挥作用的。GABA激动剂蝇蕈醇产生的效应与GABA拮抗剂相反。蝇蕈醇抑制先前暗适应视网膜中光诱导的视锥细胞收缩，并在光适应视网膜中诱导暗适应性视锥细胞伸长。这些结果表明，在绿太阳鱼视网膜中，正如其他视网膜所报道的那样，GABA抑制多巴胺释放。5 - HT在暗适应视网膜中诱导光适应性视锥细胞收缩；因此5 - HT也模拟了光或外源性应用多巴胺的作用。5 - HT的作用被舒必利、Co2 +或5 - HT拮抗剂米安色林阻断。这些结果表明，5 - HT通过刺激多巴胺释放来诱导视锥细胞收缩。褪黑素既不抑制黑暗中培养的视网膜中多巴胺诱导的视锥细胞收缩，也不诱导光照下培养的视网膜中视锥细胞伸长。我们的结果表明，GABA和5 - HT（但不是褪黑素）通过调节多巴胺释放来影响绿太阳鱼的视锥细胞视网膜运动：GABA通过抑制，5 - HT通过刺激多巴胺释放。我们在配套论文中报道多巴胺可诱导分离的视锥细胞片段收缩。综合这些观察结果强烈表明，多巴胺作为直接诱导光适应性视锥细胞视网膜运动的最终细胞外信使，而GABA和5 - HT通过调节多巴胺释放来影响这些运动。
