Pierce M E, Besharse J C
J Gen Physiol. 1985 Nov;86(5):671-89. doi: 10.1085/jgp.86.5.671.
In lower vertebrates, cone retinomotor movements occur in response to changes in lighting conditions and to an endogenous circadian clock. In the light, cone myoids contract, while in the dark, they elongate. In order to test the hypothesis that melatonin and dopamine may be involved in the regulation of cone movement, we have used an in vitro eyecup preparation from Xenopus laevis that sustains light- and dark-adaptive cone retinomotor movement. Melatonin mimics darkness by causing cone elongation. Dark- and melatonin-induced cone elongation are blocked by dopamine. Dopamine also stimulates cone contraction in dark-adapted eyecups. The effect of dopamine appears to be mediated specifically by a dopamine receptor, possibly of the D2 type. The dopamine agonist apomorphine and the putative D2 agonist LY171555 induced cone contraction. In contrast, the putative D1 agonist SKF38393-A and specific alpha 1-, alpha 2-, and beta-adrenergic receptor agonists were without effect. Furthermore, the dopamine antagonist spiroperidol not only blocked light-induced cone contraction, but also stimulated cone elongation in the light. These results suggest that dopamine is part of the light signal for cone contraction, and that its suppression is part of the dark signal for cone elongation. Melatonin may affect cone movement indirectly through its influence on the dopaminergic system.
在低等脊椎动物中,视锥细胞视网膜运动响应光照条件的变化以及内源性生物钟而发生。在光照下,视锥细胞肌样体收缩,而在黑暗中,它们伸长。为了检验褪黑素和多巴胺可能参与视锥细胞运动调节的假说,我们使用了来自非洲爪蟾的体外眼杯制备物,其能维持光适应性和暗适应性视锥细胞视网膜运动。褪黑素通过引起视锥细胞伸长来模拟黑暗。黑暗和褪黑素诱导的视锥细胞伸长被多巴胺阻断。多巴胺还刺激暗适应眼杯中的视锥细胞收缩。多巴胺的作用似乎是由一种多巴胺受体特异性介导的,可能是D2型。多巴胺激动剂阿扑吗啡和假定的D2激动剂LY171555诱导视锥细胞收缩。相比之下,假定的D1激动剂SKF38393 - A以及特异性α1 -、α2 -和β -肾上腺素能受体激动剂均无作用。此外,多巴胺拮抗剂螺哌啶醇不仅阻断光诱导的视锥细胞收缩,还在光照下刺激视锥细胞伸长。这些结果表明,多巴胺是视锥细胞收缩的光信号的一部分,其抑制是视锥细胞伸长的暗信号的一部分。褪黑素可能通过其对多巴胺能系统的影响间接影响视锥细胞运动。