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交感神经切除术和去髓鞘对胆囊收缩素-8引起的肠肌层和迷走神经背核复合体Fos样免疫反应性增加的影响。

Effect of sympathectomy and demedullation on increased myenteric and dorsal vagal complex Fos-like immunoreactivity by cholecystokinin-8.

作者信息

Raboin Shannon J, Gulley Stephen, Henley Sheryce C, Chan Wai-Chu, Esdaile Alton R, Jackson Cheryl A, Billups Leonard H, Sayegh Ayman I

机构信息

Gastroenterology Laboratory, Department of Biomedical Sciences, College of Veterinary Medicine, Tuskegee University, Tuskegee, AL 36088, United States.

出版信息

Regul Pept. 2006 May 15;134(2-3):141-8. doi: 10.1016/j.regpep.2006.02.006. Epub 2006 Apr 5.

Abstract

Chemical sympathectomy with daily, intraperitoneal (IP) injections of guanethidine sulfate to adult rats, attenuated myenteric, but not dorsal vagal complex (DVC) Fos-like immunoreactivity (Fos-LI) by cholecystokinin-8 (CCK). This technique destroys only 60-70% of the sympathetic neurons, and spares the hormonal source of catecholamines, the adrenal medulla. The goal of the current study is to evaluate the effect of complete sympathectomy or destroying 100% of the sympathetic neurons by injecting guanethidine to 1-day-old pups (40 mg/kg daily for 5 weeks), and surgically removing the adrenal medulla. In the DVC, demedullation and sympathectomy-demedullation increased Fos-LI by CCK in the area postrema and nucleus of the solitary tract, but sympathectomy-demedullation increased it only in the area postrema. In the myenteric plexus, sympathectomy increased this response in the duodenum, and demedullation increased it in the duodenum and jejunum. On the other hand, sympathectomy-demedullation attenuated myenteric Fos-LI in the jejunum. These results indicate that catecholamines may play an inhibitory role on the activation of the DVC neurons by CCK. In the myenteric neurons, however, catecholamines may have both inhibitory and excitatory roles depending on the level of the intestine e.g., duodenum vs. jejunum. This may also indicate that CCK activates the enteric neurons by different mechanisms or through different pathways.

摘要

对成年大鼠每日进行腹腔内注射硫酸胍乙啶进行化学性交感神经切除术,可减弱胆囊收缩素 -8(CCK)诱导的肌间神经丛而非迷走背核复合体(DVC)的Fos样免疫反应性(Fos-LI)。该技术仅破坏60 - 70%的交感神经元,保留了儿茶酚胺的激素来源——肾上腺髓质。本研究的目的是评估完全交感神经切除术的效果,即通过给1日龄幼崽注射胍乙啶(每日40 mg/kg,持续5周)并手术切除肾上腺髓质来破坏100%的交感神经元。在DVC中,去髓质和交感神经切除 - 去髓质增加了CCK在最后区和孤束核的Fos-LI,但交感神经切除 - 去髓质仅在最后区增加了Fos-LI。在肌间神经丛中,交感神经切除术增加了十二指肠的这种反应,而去髓质增加了十二指肠和空肠的这种反应。另一方面,交感神经切除 - 去髓质减弱了空肠的肌间神经丛Fos-LI。这些结果表明,儿茶酚胺可能对CCK激活DVC神经元起抑制作用。然而,在肌间神经元中,儿茶酚胺可能根据肠道水平(例如十二指肠与空肠)具有抑制和兴奋两种作用。这也可能表明CCK通过不同机制或不同途径激活肠神经元。

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