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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Diltiazem potentiates pentobarbital-induced hypnosis via 5-HT1A and 5-HT2A/2C receptors: role for dorsal raphe nucleus.
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Diltiazem potentiates pentobarbital-induced hypnosis via 5-HT1A and 5-HT2A/2C receptors: role for dorsal raphe nucleus.

机译：Diltiazem通过5-HT1A和5-HT2A / 2C受体引发戊巴比妥诱导的催眠：背部Raphe核的作用。

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摘要

It has been reported that the sedative component of pentobarbital is mediated by GABA receptors in an endogenous sleep pathway and the ventrolateral preoptic area (VLPO)-tuberomammillary nucleus (TMN) or VLPO-dorsal raphe nucleus (DRN) neural circuit is important in the sedative response to pentobarbital. Our previous findings indicated that the VLPO-TMN neuronal circuit may play crucial part in the augmentative effect of diltiazem on pentobarbital sleep and the serotonergic system may be involved. This study was designed to investigate the role of DRN and the serotonergic receptors 5-HT(1A) and 5-HT(2A/2C) in the augmentative effect of diltiazem on pentobarbital-induced hypnosis in rats. The results showed that diltiazem (5mg/kg, i.g.) significantly reversed pentobarbital-induced (35 mg/kg, i.p.) reduction of c-Fos expression in 5-HT neurons of DRNV (at -7.5mm Bregma), DRND, DRNVL and MRN (at -8.0mm Bregma). However it did not influence this reducing effect of pentobarbital on non-5-HT neurons either in DRN or in MRN. Moreover, the effect of diltiazem (1 or 2mg/kg, i.g.) on pentobarbital-induced (35 mg/kg, i.p.) hypnosis was significantly inhibited by 5-HT(1A) agonist 8-OH-DPAT (0.5mg/kg, i.p.) and 5-HT(2A/2C) agonist DOI (0.5mg/kg, i.p.), and potentiated by 5-HT(1A) antagonist p-MPPI (2mg/kg, i.p.) and 5-HT(2A/2C) antagonist ritanserin (2mg/kg, i.p.), respectively. From these results, it should be presumed that the augmentative effect of diltiazem on pentobarbital-induced sleep may be related to 5-HT(1A) and 5-HT(2A/2C) receptors, and DRN may be involved. In addition, it also suggested that the DRN may play a multi-modulating role in sleep-wake regulation rather than being recognized simply as arousal nuclei.
机译：据报道，戊巴比妥的镇静组分由内源性睡眠途径中的GABA受体介导，腹侧介疗区域（VLPO） - 呋喃胺核（TMN）或VLPO-背部Raphe核（DRN）神经电路在镇静中是重要的反应戊巴比妥。我们以前的研究结果表明，VLPO-TMN神经元电路可能在Diltiazem对戊巴比妥睡眠中的增强作用中起关键部分，并且可能涉及血清奈良能系统。本研究旨在探讨DRN和Serotonergic受体5-HT（1A）和5-HT（2A / 2C）在Diltiazem对大鼠戊巴比妥催眠的增强作用中的作用。结果表明，Diltiazem（5mg / kg，Ig）显着逆转戊巴比妥诱导的（35mg / kg，IP）的C-FOS表达在DRNV（在-7.5mm Bregma），Drnd，Drnvl和MRN（在-8.0mm bregma）。然而，它不会影响戊巴比妥对DRN或MRN中的非5-HER神经元的降低效果。此外，通过5-HT（1A）激动剂8-OH-DPAT（0.5mg / kg， IP）和5-HT（2A / 2C）激动剂DOI（0.5mg / kg，IP）和5-HT（1a）拮抗剂ppi（2mg / kg，IP）和5-ht（2a / 2c ）分别拮抗剂蓖麻（2mg / kg，IP）。从这些结果来看，应该推测，Diltiazem对戊巴比妥睡眠的增强效应可能与5-HT（1A）和5-HT（2A / 2C）受体相关，并且可以涉及DRN。此外，还建议DRN可以在睡眠唤醒调节中发挥多调制作用，而不是简单地识别为唤起核。

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