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红藻氨酸诱导的大鼠视网膜神经节细胞中烟碱型胆碱能受体去神经超敏反应。

Kainic acid-induced denervation supersensitivity of nicotinic, cholinergic receptors in ganglion cells of the rat retina.

作者信息

Redburn D A, Donoso J A, Mitchell C K, Gomez-Ramos P, Samson F E

出版信息

Exp Eye Res. 1984 May;38(5):449-61. doi: 10.1016/0014-4835(84)90123-4.

Abstract

The rat retina contains both nicotinic and muscarinic cholinergic receptor sites as demonstrated by specific, high affinity binding of the nicotinic ligand, [3H]-alpha-bungarotoxin, and the muscarinic ligand, [3H]-quinuclidinyl benzylate. Seven days after an intraocular injection of 5 nmol of kainic acid, nicotinic binding was increased three-fold. We suggest that nicotinic sites may be located on ganglion cells because previous studies have shown that many ganglion cells are spared after kainic acid treatment and in fact, have an increased physiological response to ACh under these conditions. The increase in nicotinic sites may reflect a supersensitivity response to the loss of acetylcholine input after the kainic acid lesion. In contrast, muscarinic binding was decreased by 70% after kainic acid treatment. These data suggest that muscarinic sites are located on amacrine cells since these cells are destroyed by kainic acid treatment and some are known to be cholino-receptive. Some of the retinal muscarinic sites may function as inhibitory autoreceptors which regulate acetylcholine release from cholinergic amacrine cells.

摘要

大鼠视网膜含有烟碱样和毒蕈碱样胆碱能受体位点,这可通过烟碱样配体[³H] -α-银环蛇毒素和毒蕈碱样配体[³H] -喹核醇基苯甲酸酯的特异性、高亲和力结合得到证明。眼内注射5纳摩尔海人酸7天后,烟碱样结合增加了两倍。我们认为烟碱样位点可能位于神经节细胞上,因为先前的研究表明,许多神经节细胞在海人酸处理后未受影响,事实上,在这些条件下它们对乙酰胆碱的生理反应增强。烟碱样位点的增加可能反映了海人酸损伤后对乙酰胆碱输入丧失的超敏反应。相比之下,海人酸处理后毒蕈碱样结合减少了70%。这些数据表明毒蕈碱样位点位于无长突细胞上,因为这些细胞会被海人酸处理破坏,并且已知其中一些是胆碱能感受性的。视网膜中的一些毒蕈碱样位点可能作为抑制性自身受体,调节胆碱能无长突细胞释放乙酰胆碱。

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