Suppr超能文献

内源性多巴胺在光照条件下抑制鸡视网膜无长突细胞中脑啡肽样免疫反应性物质的释放。

Endogenous dopamine inhibits the release of enkephalin-like immunoreactivity from amacrine cells of the chicken retina in the light.

作者信息

Boelen M K, Wellard J, Dowton M, Morgan I G

机构信息

Centre for Research on Ageing, La Trobe University, Bendigo, Vic., Australia.

出版信息

Brain Res. 1994 May 9;645(1-2):240-6. doi: 10.1016/0006-8993(94)91657-8.

Abstract

The activity of the enkephalin-immunoreactive (ENSLI) amacrine cells of the chicken retina is low in the light and high in the dark, resulting in parallel increases and decreases in the levels of the enkephalins. In vivo, the selective dopaminergic D1 antagonist SCH23390 increased the activity of the ENSLI amacrine cells in the light (ED50; 20 pmol), but had a much lesser effect in the dark, whereas the selective dopaminergic D2 antagonist sulpiride had effects only at very high concentrations (ED50; 39 nmol). In contrast, the non-selective dopamine agonist ADTN hardly affected the activity of the ENSLI amacrine cells in the light, but markedly reduced their activity in the dark. This pattern of effects suggests that dopamine actively inhibits the ENSLI amacrine cells in the light, but exerts much less inhibitory activity in the dark, consistent with the idea that dopamine is released during the exposure of the retina to light. Thus dopaminergic controls over the ENSLI amacrine cells appear to contribute to the light:dark differences in activity of the ENSLI amacrine cells. Results obtained on the dopaminergic control of enkephalin release in vitro were generally consistent with this model, except that ADTN appeared to stimulate the ENSLI amacrine cells in the dark.

摘要

鸡视网膜中脑啡肽免疫反应性(ENSLI)无长突细胞的活性在明处低而在暗处高,导致脑啡肽水平相应升高和降低。在活体中,选择性多巴胺能D1拮抗剂SCH23390在明处增加ENSLI无长突细胞的活性(半数有效剂量;20皮摩尔),但在暗处的作用小得多,而选择性多巴胺能D2拮抗剂舒必利仅在非常高的浓度下才有作用(半数有效剂量;39纳摩尔)。相反,非选择性多巴胺激动剂ADTN在明处几乎不影响ENSLI无长突细胞的活性,但在暗处显著降低其活性。这种效应模式表明,多巴胺在明处积极抑制ENSLI无长突细胞,但在暗处的抑制活性要小得多,这与多巴胺在视网膜暴露于光期间释放的观点一致。因此,多巴胺能对ENSLI无长突细胞的控制似乎导致了ENSLI无长突细胞活性的明暗差异。体外关于多巴胺能对脑啡肽释放控制的结果总体上与该模型一致,只是ADTN在暗处似乎刺激了ENSLI无长突细胞。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验