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大鼠颈上神经节中酪氨酸3-单加氧酶活性的急性跨突触调节:胆碱能和非胆碱能机制的证据

Acute transsynaptic regulation of tyrosine 3-monooxygenase activity in the rat superior cervical ganglion: evidence for both cholinergic and noncholinergic mechanisms.

作者信息

Ip N Y, Perlman R L, Zigmond R E

出版信息

Proc Natl Acad Sci U S A. 1983 Apr;80(7):2081-5. doi: 10.1073/pnas.80.7.2081.

Abstract

The rate of dopa synthesis in the rat superior cervical ganglion was increased 4- to 6-fold during continuous electrical stimulation of the cervical sympathetic trunk at 10 Hz for 30 min. This increase was only partially blocked by 3 mM hexamethonium and was not significantly affected by 6 microM atropine. In the presence of both hexamethonium and atropine, nerve stimulation still produced a 2- to 4-fold increase in dopa synthesis. Physostigmine increased dopa synthesis in both control and stimulated ganglia. This effect of physostigmine was completely blocked by hexamethonium and atropine. Dopa synthesis was also significantly increased when ganglia were incubated in a medium containing an elevated concentration of K+ (55 mM). This stimulatory effect of high K+ was totally dependent on the presence of Ca2+ in the medium, was decreased by 60% by prior decentralization of the ganglion, and was unaffected by hexamethonium and atropine. The data demonstrate that tyrosine hydroxylase activity is rapidly increased after preganglionic nerve stimulation and suggest that this increase is mediated in part by acetylcholine and in part by a second (noncholinergic) transmitter. The effects of an elevated K+ concentration may be mediated both by the release of a noncholinergic transmitter from the preganglionic nerve terminals and by direct depolarization of the ganglionic neurons.

摘要

在以10Hz的频率持续电刺激大鼠颈上交感神经干30分钟期间,颈上交感神经节中的多巴合成速率增加了4至6倍。这种增加仅部分被3mM的六甲铵阻断,并且不受6μM阿托品的显著影响。在同时存在六甲铵和阿托品的情况下,神经刺激仍使多巴合成增加2至4倍。毒扁豆碱增加了对照神经节和受刺激神经节中的多巴合成。毒扁豆碱的这种作用被六甲铵和阿托品完全阻断。当神经节在含有升高浓度K +(55mM)的培养基中孵育时,多巴合成也显著增加。高K +的这种刺激作用完全依赖于培养基中Ca2 +的存在,在神经节预先去神经支配后降低60%,并且不受六甲铵和阿托品的影响。数据表明,节前神经刺激后酪氨酸羟化酶活性迅速增加,并且表明这种增加部分由乙酰胆碱介导,部分由第二种(非胆碱能)递质介导。K +浓度升高的作用可能通过节前神经末梢释放非胆碱能递质和神经节神经元的直接去极化来介导。

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本文引用的文献

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[Metabolic requirements of sympathetic neurons].[交感神经元的代谢需求]
Cold Spring Harb Symp Quant Biol. 1952;17:245-66. doi: 10.1101/sqb.1952.017.01.023.
3
The receptor-mediated activation of tyrosine hydroxylation in the superior cervical ganglion of the rat.
J Neurochem. 1981 May;36(5):1632-40. doi: 10.1111/j.1471-4159.1981.tb00413.x.

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