Trans-synaptic induction of adrenal tyrosine hydroxylase.
Trans-synaptic induction of adrenal tyrosine hydroxylase.
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肾上腺酪氨酸羟化酶的跨突触诱导。
DOI：
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发表时间：
1969
影响因子：
3.5
通讯作者：
J. Axelrod
中科院分区：
文献类型：
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作者：
H. Thoenen;R. Mueller;J. Axelrod
6-羟基多巴胺、利血平和苯氧苯甲胺通过不同机制干扰神经节后交感神经传递，可诱导大鼠肾上腺酪氨酸羟基酶活性升高。这种儿茶酚胺合成限速酶的增加可以通过阻断供应肾上腺的内脏神经来阻止，而在切除脑垂体的动物中仍然存在这种酶活性的提高。去肾上腺神经也能部分阻止利血平和苯氧苯甲胺引起的儿茶酚胺的耗竭。结论：药物对神经节后交感神经传递的损害，导致内脏神经活动长时间反射性增强，从而导致酪氨酸羟基酶的升高。
Pretreatment of rats with 6-hydroxydopamine, reserpine and phenoxybenzamine, drugs which interfere with postganglionic sympathetic transmission by different mechanisms, induces an increase in the in vitro adrenal tyrosine hydroxylase activity. This increase in the rate-limiting enzyme in catecholamine synthesis can be prevented by interruption of the splanchnic nerves supplying the adrenal glands, whereas an elevation of the enzyme activity is still present in hypophysectomised animals. Adrenal denervation also partially prevents the depletion of catecholamines caused by reserpine and phenoxybenzamine. It is concluded that the elevation of tyrosine hydroxylase is mediated by a prolonged reflex increase in the splanchnic nerve activity as a consequence of drug-induced impairment of postganglionic sympathetic transmission.