Darmani Nissar A, Wang Yaozhi, Abad Joseph, Ray Andrew P, Thrush Gerald R, Ramirez Juan
Department of Basic Medical Sciences, College of Osteopathic Medicine of the Pacific, Western University of Health Sciences, Pomona, CA 91766, USA.
Brain Res. 2008 Jun 12;1214:58-72. doi: 10.1016/j.brainres.2008.03.077. Epub 2008 Apr 9.
Substance P (SP) is thought to play a cardinal role in emesis via the activation of central tachykinin NK1 receptors during the delayed phase of vomiting produced by chemotherapeutics. Although the existing supportive evidence is significant, due to lack of an appropriate animal model, the evidence is indirect. As yet, no study has confirmed that emesis produced by SP or a selective NK1 receptor agonist is sensitive to brain penetrating antagonists of either NK1, NK2, or NK3 receptors. The goals of this investigation were to demonstrate: 1) whether intraperitoneal (i.p.) administration of either SP, a brain penetrating (GR73632) or non-penetrating (e.g. SarMet-SP) NK1 receptor agonist, an NK2 receptor agonist (GR64349), or an NK3 receptor agonist (Pro7-NKB), would induce vomiting and/or scratching in the least shrew (Cryptotis parva) in a dose-dependent manner; and whether these effects are sensitive to the above selective receptor antagonists; 2) whether an exogenous emetic dose of SP (50 mg/kg, i.p.) can penetrate into the shrew brain stem and frontal cortex; 3) whether GR73632 (2.5 mg/kg, i.p.)-induced activation of NK1 receptors increases Fos-measured neuronal activity in the neurons of both brain stem emetic nuclei and the enteric nervous system of the gut; and 4) whether selective ablation of peripheral NK1 receptors can affect emesis produced by GR73632. The results clearly demonstrated that while SP produced vomiting only, GR73632 caused both emesis and scratching behavior dose-dependently in shrews, and these effects were sensitive to NK1-, but not NK2- or NK3-receptor antagonists. Neither the selective, non-penetrating NK1 receptor agonists, nor the selective NK2- or NK3-receptor agonists, caused a significant dose-dependent behavioral effect. An emetic dose of SP selectively and rapidly penetrated the brain stem but not the frontal cortex. Systemic GR73632 increased Fos expression in the enteric nerve plexi, the medial subnucleus of nucleus tractus solitarius, and the dorsal motor nucleus of the vagus, but not the area postrema. Ablation of peripheral NK1 receptors attenuated the ability of GR73632 to induce a maximal frequency of emesis and shifted its percent animals vomiting dose-response curve to the right. The NK1-ablated shrews exhibited scratching behavior after systemic GR73632-injection. These results, for the first time, affirm a cardinal role for central NK1 receptors in SP-induced vomiting, and a facilitatory role for gastrointestinal NK1 receptors. In addition, these data support the validation of the least shrew as a specific and rapid behavioral animal model to screen concomitantly both the CNS penetration and the antiemetic potential of tachykinin NK1 receptor antagonists.
P物质(SP)被认为在化疗药物引起的呕吐延迟期通过激活中枢速激肽NK1受体在呕吐中起主要作用。尽管现有支持证据很重要,但由于缺乏合适的动物模型,证据是间接的。迄今为止,尚无研究证实SP或选择性NK1受体激动剂引起的呕吐对NK1、NK2或NK3受体的脑穿透性拮抗剂敏感。本研究的目的是证明:1)腹腔注射SP、脑穿透性(GR73632)或非穿透性(如SarMet-SP)NK1受体激动剂、NK2受体激动剂(GR64349)或NK3受体激动剂(Pro7-NKB)是否会以剂量依赖性方式诱导最小鼩鼱(Cryptotis parva)呕吐和/或抓挠行为;以及这些效应是否对上述选择性受体拮抗剂敏感;2)外源性催吐剂量的SP(50mg/kg,腹腔注射)是否能穿透鼩鼱脑干和额叶皮质;3)GR73632(2.5mg/kg,腹腔注射)诱导的NK receptors activation是否会增加脑干催吐核和肠道肠神经系统神经元中Fos测量的神经元活性;4)选择性切除外周NK1受体是否会影响GR73632引起的呕吐。结果清楚地表明,虽然SP仅引起呕吐,但GR73632在鼩鼱中剂量依赖性地引起呕吐和抓挠行为,并且这些效应对NK1受体拮抗剂敏感,但对NK2或NK3受体拮抗剂不敏感。选择性非穿透性NK1受体激动剂以及选择性NK2或NK3受体激动剂均未引起显著的剂量依赖性行为效应。催吐剂量的SP选择性且迅速地穿透脑干,但未穿透额叶皮质。全身性GR73632增加了肠神经丛、孤束核内侧亚核和迷走神经背运动核中Fos的表达,但未增加最后区的Fos表达。切除外周NK1受体减弱了GR73632诱导最大呕吐频率的能力,并使其呕吐动物百分比剂量反应曲线向右移动。NK1切除的鼩鼱在全身性注射GR73632后表现出抓挠行为。这些结果首次证实了中枢NK1受体在SP诱导的呕吐中的主要作用,以及胃肠道NK1受体的促进作用。此外,这些数据支持将最小鼩鼱作为一种特异性和快速行为动物模型用于同时筛选速激肽NK1受体拮抗剂的中枢神经系统穿透性和止吐潜力的验证。