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[中缝大核、蓝斑和迷走神经背运动核在胃动力下行调节中的关系]

[The relationships among raphe magnus nucleus, locus coeruleus and dorsal motor nucleus of vagus in the descending regulation of gastric motility].

作者信息

Qiao Hui, An Shu-Cheng, Xu Chang

机构信息

Department of Life Science, Shanxi Normal University, Xi' an 710062, China.

出版信息

Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2011 Feb;27(1):124-8.

Abstract

OBJECTIVE

To explore the interrelationship among dorsal motor nucleus of the vagus (DMV), locus coeruleus (LC) and raphe magnus nucleus (NRM) in the mechanism of the descending regulation on gastric motility, which may constitute a parasympathetic local circuit, work as a neural center of gastric modulation in brainstem.

METHODS

Using nucleus location, electric stimulation and lesion, together with microinjection, and recording the inter-gastric pressure.

RESULTS

(1) LC stimulation could inhibit the gastric motility significantly (P < 0.01), DMV lesion weaken this effect, while blocking the a receptor on DMV could reverse the effect. (2) NRM stimulation reduced the amplitude of gastric constriction (P < 0.01), DMV lesion could abolish the effect, but blocking the 5-HT2A receptor on DMV depressed the gastric motility heavily (P < 0.01) like NRM stimulation. While LC lesion could abolish the effect of NRM stimulation, and microinjection of ritanserin into LC could likewise abolish it.

CONCLUSION

(1) LC inhibit the gastric motility via a receptor in DMV, and meanwhile may excite it through 5-HT2A receptor in DMV, these two ways work together to keeping the gastric motility amplitude normally. (2) NRM inhibit the gastric motility via 5-HT2A receptor in LC.

摘要

目的

探讨迷走神经背核(DMV)、蓝斑(LC)和中缝大核(NRM)在胃动力下行调节机制中的相互关系,它们可能构成一个副交感神经局部回路,作为脑干中胃调节的神经中枢。

方法

采用核团定位、电刺激、损毁,结合微量注射,并记录胃内压。

结果

(1)刺激LC可显著抑制胃动力(P<0.01),损毁DMV可减弱此效应,而阻断DMV上的α受体可逆转该效应。(2)刺激NRM可降低胃收缩幅度(P<0.01),损毁DMV可消除该效应,但阻断DMV上的5-HT2A受体可使胃动力显著降低(P<0.01),类似于刺激NRM。而损毁LC可消除NRM刺激的效应,向LC内微量注射利坦色林同样可消除该效应。

结论

(1)LC通过DMV上的α受体抑制胃动力,同时可能通过DMV上的5-HT2A受体兴奋胃动力,这两种方式共同作用以维持胃动力幅度正常。(2)NRM通过LC上的5-HT2A受体抑制胃动力。

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