Reversal of noradrenergic depletion and lipid peroxidation in the pons after brain injury correlates with motor function recovery in rats

Reversal of noradrenergic depletion and lipid peroxidation in the pons after brain injury correlates with motor function recovery in rats
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DOI:
10.1016/j.neulet.2008.07.046
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发表时间:
2008-09-26
影响因子:
2.5
通讯作者:
Gonzalez-Pina, Rigoberto
Gonzalez-Pina, Rigoberto
中科院分区:
医学4区
文献类型:
--
作者:
Bueno-Nava, Antonio;Montes, Sergio;Gonzalez-Pina, Rigoberto

文献摘要

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脑损伤后的功能障碍被归因于与损伤部位相关的区域的抑制。因此,去甲肾上腺素(NA)被认为在运动损伤的恢复中起着关键作用。然而,这一恢复过程的机制尚未完全阐明。此外,蓝斑(LC)从脑桥通过大鼠感觉运动皮质投射,损伤使LC纤维切断,抑制NA功能。这是通过测量感觉运动皮质损伤后脑桥中的脂质过氧化(LP)来检验的。脑桥功能的抑制预计会改变接受脑桥传出的区域。雄性Wistar大鼠分为对照组(n=16)、损伤组(n=10)和恢复组(n=16),分别于伤后2~20d行束走试验。我们测量了脑桥和小脑两侧的NA和LP。我们发现,损伤动物脑桥和小脑中NA减少,运动缺陷和脑桥Lp增加。恢复期大鼠的NA和Lp水平与对照组非常相似。这些观察结果表明,脑损伤后远距离抑制的机制与脂质过氧化有关,损伤动物小脑NA的减少是由脑桥或接受脑桥NA投射的区域的去甲肾上腺素能抑制所介导的。(C)2008爱思唯尔爱尔兰有限公司。保留所有权利。
Functional impairment after brain injury (BI) has been attributed to the inhibition of regions that are related to the injured site. Therefore, noradrenaline (NA) is thought to play a critical role in recovery from motor injury. However, the mechanism of this recovery process has not been completely elucidated. Moreover, the locus coeruleus (LC) projects from the pons through the rat sensorimotor cortex, and injury axotomizes LC fibers, depressing NA function. This was tested by measuring lipid peroxidation (LP) in the pons after sensorimotor cortex injury. Depression of function in the pons would be expected to alter areas receiving pontine efferents. Male Wistar rats were divided into three groups: control (n=16), injured (n=10) and recovering (n=16), and they were evaluated using a beam-walking assay between 2 and 20 days after cortical injury. We performed measures of NA and LP in both sides of the pons and cerebellum. We found a decrease of NA in the pons and the cerebellum, and a concomitant increase in the motor deficit and LP in the pons of injured animals. Recovering rats had NA and LP levels that were very similar to those observed in control rats. These observations suggest that the mechanism of remote inhibition after BI involves lipid peroxidation, and that the NA decrease found in the cerebellum of injured animals is mediated by a noradrenergic depression in the pons, or in areas receiving NA projections from the pons. (C) 2008 Elsevier Ireland Ltd. All rights reserved.