ADENOSINE DERIVATIVES AND CHOLINERGIC NERVE ENDINGS

这个项目的目的是进一步研究腺苷的参与。 外周胆碱能神经末梢功能的衍生物 神经系统。关于腺嘌呤核苷酸的释放，是 所有形式的乙酰胆碱(ACh)分泌和 三磷酸腺苷(ATP)的释放。具体而言，ACH版本 将通过各种方法诱发，并测定ATP和ACh的释放。 将使用生物测定化学方法来检测ACh的释放和 用萤火虫生物发光反应检测ATP的释放。使用 关于腺苷衍生物的作用，一种电生理学 将对ACh的释放进行研究，以表征特定的腺苷 介导抑制和促进运动中ACh释放的受体 神经末梢和可能的腺苷磷酸受体抑制 神经节前神经末梢的ACh释放。的效力序列 各种激动剂和拮抗剂及其与腺苷和 嘌呤能受体激活和细胞内调节剂，如钙和 将对环核苷酸进行研究。脂质体将作为一种 将钙或嘌呤衍生物输送到神经细胞质的途径 结束了。因为腺嘌呤核苷酸代谢异常会以某些形式发生 肌肉疾病(如Duchenne营养不良)，ACh释放在 神经节在家族性自主神经紊乱中的作用 腺苷衍生物和神经肌肉功能应该提供有价值的 未来对病态胆碱能突触的研究框架。

The aim of this project is to study further the involvement of adenosine derivatives in the function of cholinergic nerve endings in the peripheral nervous system. With respect to the release of adenine nucleotide, is there an association between all forms of acetylcholine (ACh) secretion and the release of adenosine triphosphate (ATP). Specifically, ACh release will be evoked by various methods and the release of ATP and ACh assayed. Bioassay chemical methods will be used to detect ACh release and the firefly bioluminescence reaction employed to detect ATP release. With respect to the effects of adenosine derivatives, an electrophysiological study of ACh release will be made to characterize the specific adenosine receptors that mediate inhibition and enhancement of ACh release at motor nerve endings and the putative adenosine phosphate receptors that inhibit ACh release at preganglionic nerve endings. The potency sequences for various agonists and antagonists and the relationship between adenosine or purinergic receptor activation and intracellular modulators such as Ca and cyclic necleotides will be investigated. Liposomes will be employed as a means of delivering Ca or purine derivatives to the cytoplasm of the nerve ending. As abnormal adenine necleotide metabolism occurs in certain forms of muscle disease (e.g. Duchenne dystrophy), and ACh release is impaired at ganglia in familial dysautonomia, studying the normal relationship between adenosine derivatives and neuromuscular function should provide a valuable framework for future studies on the diseased cholinergic synapses.