Del Bianco E, Maggi C A, Santicioli P, Geppetti P
Institute of Clinical Dermatology, Florence University, Italy.
Neurosci Lett. 1994 Mar 28;170(1):163-6. doi: 10.1016/0304-3940(94)90264-x.
Electrical field stimulation (EFS) and bradykinin (BK) are able to activate capsaicin-sensitive sensory neurons of guinea-pig atria in a omega-conotoxin (CTX)-sensitive and Ruthenium Red (RR)-insensitive manner. The aim of this work was to study EFS and BK-induced release of calcitonin gene-related peptide (CGRP) from guinea-pig atria and in particular the action of morphine and neuropeptide Y (NPY) on this release. EFS-induced CGRP release was frequency-dependent and tetrodotoxin (TTX)-sensitive, while BK-evoked CGRP release was TTX-insensitive. On the other hand, CGRP outflow induced by either EFS or BK was similarly reduced in the presence of morphine and NPY. It is therefore hypothesized that NPY and opioids exert their inhibitory action by acting on the very terminal region of the nerve fibre. Moreover, our results show that dermorphine but not dynorphin reduced BK-evoked CGRP release, suggesting that mu opioid receptors are responsible for morphine action. Studying the action of peptide YY and NPY(16-36) on BK-evoked CGRP release, we demonstrated that both had similar inhibitory effects, supporting the presence of Y2 receptors on the nerve terminal region.
电场刺激（EFS）和缓激肽（BK）能够以一种对ω-芋螺毒素（CTX）敏感而对钌红（RR）不敏感的方式激活豚鼠心房的辣椒素敏感感觉神经元。这项工作的目的是研究EFS和BK诱导的豚鼠心房降钙素基因相关肽（CGRP）的释放，特别是吗啡和神经肽Y（NPY）对这种释放的作用。EFS诱导的CGRP释放是频率依赖性的且对河豚毒素（TTX）敏感，而BK诱发的CGRP释放对TTX不敏感。另一方面，在吗啡和NPY存在的情况下，EFS或BK诱导的CGRP流出同样减少。因此推测NPY和阿片类药物通过作用于神经纤维的非常末端区域发挥其抑制作用。此外，我们的结果表明，皮啡肽而非强啡肽减少了BK诱发的CGRP释放，表明μ阿片受体负责吗啡的作用。研究肽YY和NPY（16 - 36）对BK诱发的CGRP释放的作用，我们证明两者具有相似的抑制作用，支持神经末梢区域存在Y2受体。
