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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Noradrenaline release-inhibiting receptors on PC12 cells devoid of alpha(2(-)) and CB(1) receptors: similarities to presynaptic imidazoline and edg receptors.
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Noradrenaline release-inhibiting receptors on PC12 cells devoid of alpha(2(-)) and CB(1) receptors: similarities to presynaptic imidazoline and edg receptors.

机译：不含α（2（-））和CB（1）受体的PC12细胞上的去甲肾上腺素释放抑制受体：与突触前咪唑啉和edg受体相似。

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摘要

The aim of the present study was to classify release-inhibiting receptors on rat pheochromocytoma PC12 cells. Veratridine-evoked [3H]noradrenaline release from PC12 cells was inhibited by micromolar concentrations of the imidazoline and guanidine derivatives cirazoline, clonidine, aganodine, 1,3-di(2-tolyl)guanidine, BDF6143 and agmatine, and of the cannabinoid receptor agonist WIN55,212-2 (R(+)-[2,3-dihydro-5-methyl-3-[(morpholinyl)methyl]pyrrolo-[1,2,3-de]-1,4- benzoxazin-yl](1-naphthalenyl)methanone mesylate), but not by noradrenaline. The inhibitory effect of clonidine was antagonized by micromolar concentrations of rauwolscine and SR141716A (N-[piperidin-1-yl]-5-[4-chlorophenyl]-1-[2,4-dichlorophenyl]-4-methyl-1H- pyrazole-3-carboxamide). The potencies of the agonists and antagonists were compatible with an action at previously characterized presynaptic imidazoline receptors. 1-Oleoyl-lysophosphatidic acid, but not sphingosine-1-phosphate, produced an inhibition of release that was antagonized by 30 microM rauwolscine, 1 microM SR141716A and 10 microM LY320135 as well as by pretreatment of the cells with 100 microM clonidine for 72 h. Polymerase chain reaction (PCR) experiments on cDNA from PC12 mRNA suggest mRNA expression of lysophospholipid receptors encoded by the genes edg2, edg3, edg5 and edg7, but not of receptors encoded by edg1, edg4, edg6 and edg8, and not of alpha(2A(-))nd CB(1) receptors. In conclusion, PC12 cells are not endowed with alpha(2)-adrenoceptors and CB(1) cannabinoid receptors, but with an inhibitory receptor recognizing imidazolines, guanidines and WIN55,212-2 similar to that on sympathetic nerves. The PCR results and the ability of 1-oleoyl-LPA to mimic these drugs (also with respect to their susceptibility to antagonists) suggest that the release-inhibiting receptor may be an edg-encoded lysophospholipid receptor.
机译：本研究的目的是对大鼠嗜铬细胞瘤PC12细胞上的释放抑制受体进行分类。咪唑啉和胍衍生物西拉唑啉，可乐定，金刚烷胺，1,3-二（2-甲苯基）胍，BDF6143和胍丁胺以及大麻素受体激动剂的微摩尔浓度抑制了Vertraridine诱发的[3H]去甲肾上腺素从PC12细胞的释放WIN55,212-2（R（+）-[2,3-二氢-5-甲基-3-[（吗啉基）甲基]吡咯并-[1,2,3-de] -1,4-苯并恶嗪-基] （1-萘甲磺酸甲磺酸酯），但不是去甲肾上腺素。微摩尔浓度的鼠李糖和SR141716A（N- [哌啶-1-基] -5- [4-氯苯基] -1- [2,4-二氯苯基] -4-甲基-1H-吡唑）拮抗可乐定的抑制作用-3-羧酰胺）。激动剂和拮抗剂的效力与对先前表征的突触前咪唑啉受体的作用相容。 1-油酰基-溶血磷脂酸而不是鞘氨醇-1-磷酸产生抑制释放的作用，该抑制作用被30 microM狼wol素，1 microM SR141716A和10 microM LY320135拮抗，以及用100 microM可乐定预处理细胞72小时。对PC12 mRNA cDNA的聚合酶链反应（PCR）实验表明，由edg2，edg3，edg5和edg7基因编码的溶血磷脂受体的mRNA表达，但不是由edg1，edg4，edg6和edg8编码的受体，而不是alpha（2A） （-））个CB（1）受体。总之，PC12细胞不具有alpha（2）-肾上腺素能受体和CB（1）大麻素受体，但具有与咪唑啉，胍和WIN55,212-2相似的抑制性受体，与交感神经相似。 PCR结果和1-油基-LPA模仿这些药物的能力（也就其对拮抗剂的敏感性而言）表明，释放抑制受体可能是一种经edg编码的溶血磷脂受体。

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