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首页> 外文期刊>Life sciences >Nociceptin and dynorphin A(1-17) produce antianalgesia through independent systems in mice.
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Nociceptin and dynorphin A(1-17) produce antianalgesia through independent systems in mice.

机译：Nociceptin和强啡肽A（1-17）通过独立的系统在小鼠中产生抗痛觉过敏。

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摘要

The administration of dynorphin A(1-17), Dyn, intrathecally (i.t.) or of nociceptin, intracerebroventricularly (i.c.v.) produces antianalgesic actions against i.t. morphine in the tail flick test in mice. The antianalgesic action of nociceptin is mediated by spinal PGE2 and attenuated by i.t. PGD2 or indomethacin. The Dyn response is mediated by release of IL1beta in the spinal cord to activate an ascending pathway to the brain and in turn releases IL1beta in the brain which activates a descending pathway to the spinal cord. The present work investigated the possibility that the action of IL1beta in the Dyn system might release prostaglandins so that the Dyn and nociceptin antianalgesic systems would overlap at these points. The results indicated that in the Dyn system neither the IL1beta in the spinal cord or brain implicated prostaglandin release because i.t. and i.c.v. PGD2 and indomethacin did not affect Dyn-induced antianalgesia. In addition, nociceptin-induced antianalgesia did not involve components in the Dyn system. Thus, the Dyn and nociceptin antianalgesic systems did not overlap and each were independent systems.
机译：鞘内（i.t.）给予Dyn强啡肽A（1-17）或脑室内（i.c.v.）给予诺西汀可产生抗i.t.吗啡在小鼠的甩尾试验中。 Nociceptin的抗镇痛作用是由脊柱PGE2介导的，并被i.t.减弱。 PGD​​2或消炎痛。 Dyn反应由脊髓中IL1beta的释放介导，从而激活了通往大脑的上升途径，进而释放了大脑中的IL1beta，从而激活了向脊髓的下降途径。目前的工作调查了Dyn系统中IL1β的作用可能释放前列腺素的可能性，以使Dyn和伤害感受药抗痛药系统在这些位置重叠。结果表明，在Dyn系统中，脊髓或大脑中的IL1β均不涉及前列腺素的释放，因为和i.c.v. PGD​​2和消炎痛不影响Dyn诱导的抗痛觉过敏。此外，伤害感受肽诱导的镇痛不涉及Dyn系统中的成分。因此，Dyn和伤害感受肽止痛系统不重叠，并且各自为独立系统。

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