Veterans Affairs Medical Center, Oklahoma City, OK, USA.
Neurogastroenterol Motil. 2012 Mar;24(3):283-7, e112. doi: 10.1111/j.1365-2982.2011.01849.x. Epub 2011 Dec 21.
Copper deficiency affects the peripheral (PNS) and central (CNS) nervous systems and can lead to neurological deficits in humans. No studies have addressed whether copper deficiency affects the enteric nervous system (ENS). We hypothesized that ENS abnormalities impair intestinal function in copper deficiency.
We induced copper deficiency in rats by nutritional deprivation. Once hypocupremia was achieved, we euthanized the animals and harvested the small and large intestine. The longitudinal smooth muscle from the jejunum and colon was suspended in organ baths and contractility in response to electrical field stimulation (EFS) was assessed. Mucosa was also isolated from each region and placed into modified Ussing chambers to determine whether the copper deficiency leads to alterations in epithelial transport measured as a change in short circuit current across the mucosa in response to EFS.
A copper deficient diet (CDD) in normal rats for 9 weeks was sufficient to produce hypocupremia. Colonic smooth muscle contractility was significantly decreased in response to EFS in rats fed a CDD compared with controls, however, jejunal smooth muscle contractility in response to EFS in rats fed a CDD rats resembled that observed in controls. No significant changes in secretory function were observed in either region in response to CDD.
CONCLUSIONS & INFERENCES: Dietary copper deficiency produces significant changes in the neural regulation of colonic smooth muscle contractility in a rodent model. Thus, along with CNS and PNS effects in humans, copper deficiency results in abnormal ENS regulation of intestinal function in rats.
铜缺乏会影响周围神经系统（PNS）和中枢神经系统（CNS），并可能导致人类出现神经功能缺陷。目前尚无研究探讨铜缺乏是否会影响肠神经系统（ENS）。我们假设 ENS 异常会损害铜缺乏症大鼠的肠道功能。
我们通过营养剥夺诱导大鼠铜缺乏。一旦出现低铜血症，我们便处死动物并采集小肠和大肠。将空肠和结肠的纵行平滑肌悬浮在器官浴中，评估其对电刺激（EFS）的收缩反应。还从每个区域分离黏膜，并将其放入改良的 Ussing 室中，以确定铜缺乏是否会导致上皮转运的改变，即 EFS 引起的黏膜短电流的变化。
正常大鼠给予铜缺乏饮食（CDD） 9 周足以导致低铜血症。与对照组相比，CDD 喂养大鼠的结肠平滑肌对 EFS 的收缩反应明显减弱，但 CDD 喂养大鼠的空肠平滑肌对 EFS 的收缩反应类似于对照组。在这两个区域，对 CDD 的反应均未观察到分泌功能的显著变化。
饮食铜缺乏在大鼠模型中产生了对结肠平滑肌收缩的神经调节的显著变化。因此，除了人类的 CNS 和 PNS 效应外，铜缺乏还导致大鼠 ENS 对肠道功能的调节异常。
