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热量限制并不能抵消运动神经元生物物理特性中与年龄相关的变化。

Caloric restriction does not offset age-associated changes in the biophysical properties of motoneurons.

作者信息

Kalmar Jayne M, Button Duane C, Gardiner Kalan, Cahill Farrell, Gardiner Phillip F

机构信息

Spinal Cord Research Center, Department of Physiology, University of Manitoba, 730 William Ave., 436 BMSB, Winnipeg, Manitoba R3E 3J7, Canada.

出版信息

J Neurophysiol. 2009 Feb;101(2):548-57. doi: 10.1152/jn.90617.2008. Epub 2008 Sep 10.

Abstract

Age-associated changes in neuromuscular function may be due to a loss of motor neurons as well as changes in their biophysical properties. Neuronal damage imposed by reactive oxygen species may contribute to age-related deficits in CNS function. Thus we hypothesized that aging would alter the functional properties of motoneurons and that caloric-restriction would offset these changes. Intracellular recordings were made from lumbar motoneurons of old Fisher Brown Norway (FBN) fed ad libitum (oldAL, 30.8+/-1.3 mo) or on a fortified calorie-restricted diet from 14 wk of age (oldCR, 31.0+/-1.8 mo). Basic and rhythmic firing properties recorded from these aged motoneurons (MNs) were compared with properties recorded from young FBN controls (young, 8.4+/-4.6 mo). Compared with young MNs, old MNs had a 104% greater (P<0.001) afterhyperpolarization potential (AHP), a 21.1% longer AHP half-decay time (P<0.05), 28.7% lower rheobase (P<0.001), 49.7% greater (P<0.001) input resistance, 21.1% (P<0.0001) less spike frequency adaptation, lower minimal (30.2%, P<0.0001) and maximal (16.7%, P<0.0001) steady-state firing frequencies, a lower (35.5%, P<0.0001) frequency-current slope, and an increased incidence of persistent inward current. Because basic properties became more diverse in old MNs and the slope of the frequency-current relationship, which is normally similar for high- and low-threshold MNs, was lower in the old group, we conclude that aging alters the biophysical properties of MNs in a fashion that cannot be simply attributed to a loss of high-threshold MNs. Surprisingly, caloric restriction, which is known to attenuate aging-associated changes in hindlimb muscles, had no effect on the progress of aging in the innervating MNs.

摘要

神经肌肉功能的年龄相关变化可能是由于运动神经元的丧失以及它们生物物理特性的改变。活性氧引起的神经元损伤可能导致中枢神经系统功能的年龄相关缺陷。因此,我们假设衰老会改变运动神经元的功能特性,而热量限制会抵消这些变化。对随意进食的老年费希尔·布朗挪威大鼠(FBN)(老年自由进食组,30.8±1.3个月)或从14周龄开始接受强化热量限制饮食的老年大鼠(老年热量限制组,31.0±1.8个月)的腰段运动神经元进行细胞内记录。将这些老年运动神经元(MNs)记录的基本和节律性放电特性与年轻FBN对照组(年轻组,8.4±4.6个月)记录的特性进行比较。与年轻MNs相比,老年MNs的超极化后电位(AHP)大104%(P<0.001),AHP半衰期长21.1%(P<0.05),阈强度低28.7%(P<0.001),输入电阻大49.7%(P<0.001),放电频率适应性低21.1%(P<0.0001),最小(30.2%,P<0.0001)和最大(16.7%,P<0.0001)稳态放电频率低,频率-电流斜率低(35.5%,P<0.0001),持续性内向电流发生率增加。由于老年MNs的基本特性变得更加多样化,并且频率-电流关系的斜率(高阈值和低阈值MNs通常相似)在老年组中较低,我们得出结论,衰老以一种不能简单归因于高阈值MNs丧失的方式改变了MNs的生物物理特性。令人惊讶的是,已知能减轻后肢肌肉衰老相关变化的热量限制,对支配MNs的衰老进程没有影响。

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