The effect of supramaximal electric field stimulation on 3H released from rat spleen strips was studied after loading with either [3H]dopamine ([3H]DA) or [3H]norepinephrine ([3H]NE). In some experiments, [3H]DA and [3H]NE stored in the tissue or released in response to electrical stimulation were separated from their tritiated metabolites using HPLC followed by radiochemical detection. The stimulation-evoked release of 3H after loading with either derivative was subject to negative feedback modulation through alpha2-adrenergic, D2-dopamine and muscarinic acetylcholine receptors, and could be prevented by either calcium removal or tetrodotoxin blocking of Na+ influx, indicating its neuronal and vesicular origin. After the separation of radioactive metabolites by HPLC, both the tissue loaded with [3H]DA and the fractions collected during electrical stimulation contained a considerable amount of [3H]NE, providing evidence that the neurons it originated from were adrenergic in function. [3H]DA was also released during electrical stimulation. Since the spleen does not receive dopaminergic innervation, it was concluded that the noradrenergic axon terminals in the spleen were able to take up DA, convert it in part into NE, and release it as both DA and NE in response to neural activity. The ratio of [3H]DA and [3H]NE in the spleen loaded with [3H]DA was found to be dependent on both temperature and time of loading, and could be modulated by various drugs such as desmethylimipramine, a NE uptake blocker, and disulfiram or fusaric acid, dopamine beta-hydroxylase inhibitors. The phenomenon may reveal a new mechanism by which immunocytes in the spleen can be regulated by the neuroendocrine system.

译文

在装载[3H]多巴胺([3H] DA)或[3H]去甲肾上腺素([3H] NE)后,研究了超最大电场刺激对大鼠脾脏条带释放的3H的影响。在某些实验中,使用HPLC随后进行放射化学检测,将stored 3] DA和[3 H] NE存储在组织中或响应电刺激释放而从tri化代谢产物中分离出来。装载任何一种衍生物后,刺激诱发的3H释放均通过α2-肾上腺素,D2-多巴胺和毒蕈碱型乙酰胆碱受体受到负反馈调节,并且可以通过除钙或河豚毒素对Na流入的阻滞来阻止,表明其神经元和水泡起源。通过HPLC分离放射性代谢物后,装载有[3H] DA的组织和在电刺激过程中收集的馏分均含有大量的[3H] NE,这提供了其起源的神经元在功能上具有肾上腺素能的证据。在电刺激过程中也释放了[3H] DA。由于脾脏不接受多巴胺能神经支配,因此得出的结论是,脾脏中的去甲肾上腺素能轴突末端能够吸收DA,将其部分转化为NE,并将其作为DA和NE释放,以响应神经活动。发现负载有[3H] DA的脾脏中[3H] DA和[3H] NE的比例取决于温度和加载时间,并且可以通过各种药物(例如去甲丙咪嗪,一种NE吸收阻断剂,和双硫仑或富马酸,多巴胺β-羟化酶抑制剂。这种现象可能揭示了一种新的机制,脾脏中的免疫细胞可以被神经内分泌系统调节。

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