MacDonell Christopher W, Chopek Jeremy W, Gardiner Kalan R, Gardiner Phillip F
Spinal Cord Research Centre, Department of Physiology & Pathophysiology, Rady Faculty of Health, University of Manitoba, Winnipeg, Manitoba, Canada
Spinal Cord Research Centre, Department of Physiology & Pathophysiology, Rady Faculty of Health, University of Manitoba, Winnipeg, Manitoba, Canada.
J Neurophysiol. 2017 Oct 1;118(4):2318-2327. doi: 10.1152/jn.00423.2017. Epub 2017 Jul 26.
Small-diameter sensory dysfunction resulting from diabetes has received much attention in the literature, whereas the impact of diabetes on α-motoneurons (MN) has not. In addition, the chance of developing insulin resistance and diabetes is increased in obesity. No study has examined the impact of obesity or diabetes on the biophysical properties of MN. Lean Zucker rats and Zucker diabetic fatty (ZDF) rats were separated into lean, obese (ZDF fed standard chow), and diabetic (ZDF fed high-fat diet that led to diabetes) groups. Glass micropipettes recorded hindlimb MN properties from identified flexor and extensor MN. MN were separated within their groups on the basis of input conductance, which created high- and low-input conductance subpopulations for each. A significant shorter (20%) afterhyperpolarization half-decay (AHP) was found in low-conductance MN for the diabetic group only, whereas AHP½ tended to be shorter in the obese group (19%). Significant positive correlations were found among rheobase and input conductance for both lean and obese animals. No differences were found between the groups for afterhyperpolarization amplitude (AHP), input conductance, rheobase, or any of the rhythmic firing properties (frequency-current slope and spike-frequency adaptation index). MN properties continue to be heterogeneous in obese and diabetic animals. Obesity does not seem to influence lumbar MN. Despite the resistance of MN to the impact of diabetes, the reduced AHP decay and the tendency for a reduction in AHP may be the first sign of change to MN function. Knowledge about the impact of obesity and diabetes on the biophysical properties of motoneurons is lacking. We found that diabetes reduces the duration of the afterhyperpolarization and that motoneuron function is unchanged by obesity. A reduced afterhyperpolarization may impact discharge characteristics and may be the first sign of change to motoneuron function.
糖尿病导致的小直径感觉功能障碍在文献中受到了广泛关注，而糖尿病对α运动神经元（MN）的影响却未得到充分研究。此外，肥胖会增加患胰岛素抵抗和糖尿病的几率。尚无研究探讨肥胖或糖尿病对运动神经元生物物理特性的影响。将瘦素 Zucker 大鼠和 Zucker 糖尿病脂肪（ZDF）大鼠分为瘦素组、肥胖组（ZDF 喂食标准饲料）和糖尿病组（ZDF 喂食导致糖尿病的高脂肪饮食）。玻璃微电极记录了已识别的屈肌和伸肌运动神经元的后肢运动神经元特性。根据输入电导将运动神经元在其组内进行分类，从而为每组创建高输入电导和低输入电导亚群。仅在糖尿病组的低电导运动神经元中发现超极化后电位半衰期（AHP）显著缩短（20%），而肥胖组的 AHP½ 则有缩短趋势（19%）。在瘦素组和肥胖组动物中，阈强度与输入电导之间均存在显著正相关。在超极化后电位幅度（AHP）、输入电导、阈强度或任何节律性放电特性（频率-电流斜率和放电频率适应指数）方面，各组之间均未发现差异。肥胖和糖尿病动物的运动神经元特性仍然存在异质性。肥胖似乎不会影响腰段运动神经元。尽管运动神经元对糖尿病的影响具有抗性，但 AHP 衰减的降低以及 AHP 降低的趋势可能是运动神经元功能改变的首个迹象。目前缺乏关于肥胖和糖尿病对运动神经元生物物理特性影响的相关知识。我们发现糖尿病会缩短超极化后电位的持续时间，而肥胖对运动神经元功能没有影响。超极化后电位的缩短可能会影响放电特性，并且可能是运动神经元功能改变的首个迹象。
