Blanco Jennifer E, Anderson Kim D, Steward Oswald
Department of Anatomy, University of California at Irvine School of Medicine, CA 92697-4292, USA.
Exp Neurol. 2007 Feb;203(2):333-48. doi: 10.1016/j.expneurol.2006.08.017. Epub 2006 Oct 16.
Previous studies using a grip strength meter (GSM) revealed a loss of gripping ability following cervical hemisection injuries in mice, followed by partial recovery. Here, we assess whether normal gripping ability and the recovered gripping ability after cervical hemisection depend on the cerebral cortex. First, we assessed grip strength of both forepaws of 18-week-old C57Bl/6 mice before and after a left sensorimotor cortex lesion or right lateral hemisection at C5. Both lesions led to a complete loss of gripping ability by the right forepaw and caused only minor deficits in the left. After cortical lesions, gripping ability re-appeared at about 17 days post-injury, and grip strength recovered to near-normal levels by 24 days post-injury. After C5 hemisections, gripping ability re-appeared after 31 days post-injury in 50% of the mice. Follow-up experiments were then carried out in which 10-week-old mice received C4 hemisection injuries and were tested for 28 days; then mice received secondary lesions of the sensorimotor cortex ipsi- or contralateral to the hemisection. Younger mice with cervical hemisections recovered gripping ability between 12 and 28 days post-hemisection. Cortical lesions on the side contralateral to the hemisection led to a complete loss of recovered gripping ability in all mice; cortical lesions on the side ipsilateral to the hemisection also disrupted recovered gripping ability in some animals. Surprisingly, lesions of the cortex ipsilateral to the hemisection did not impair gripping ability of the contralateral (left) forepaw. Finally, we assessed the effects of a third lesion of whichever side of the sensorimotor cortex remained, so that the sensorimotor cortex was ablated bilaterally. Remarkably, gripping function by the forepaw contralateral to the original hemisection was completely unaffected, and the recovered gripping function by the forepaw ipsilateral to the hemisection was disrupted in only some of the animals. These results indicate a substantial reorganization of motor control of gripping function after cervical injuries in mice so that gripping ability by both forepaws becomes largely independent of cortical control.
先前使用握力计（GSM）进行的研究表明，小鼠在颈椎半切损伤后握力会丧失，随后部分恢复。在此，我们评估颈椎半切后正常的握力以及恢复后的握力是否依赖于大脑皮层。首先，我们评估了18周龄C57Bl/6小鼠在左侧感觉运动皮层损伤或C5右侧半切前后两只前爪的握力。两种损伤均导致右前爪握力完全丧失，而左前爪仅有轻微缺陷。皮层损伤后，握力在损伤后约17天重新出现，到损伤后24天握力恢复到接近正常水平。C5半切后，50%的小鼠在损伤后31天握力重新出现。随后进行了后续实验，10周龄小鼠接受C4半切损伤并测试28天；然后小鼠接受半切同侧或对侧感觉运动皮层的二次损伤。颈椎半切的年轻小鼠在半切后12至28天恢复握力。半切对侧的皮层损伤导致所有小鼠恢复的握力完全丧失；半切同侧的皮层损伤也在一些动物中破坏了恢复的握力。令人惊讶的是，半切同侧的皮层损伤并未损害对侧（左）前爪的握力。最后，我们评估了感觉运动皮层剩余一侧的第三次损伤的影响，从而双侧切除感觉运动皮层。值得注意的是，原始半切对侧前爪的抓握功能完全未受影响，半切同侧前爪恢复的抓握功能仅在部分动物中受到破坏。这些结果表明，小鼠颈椎损伤后抓握功能的运动控制发生了实质性重组，使得两只前爪的抓握能力在很大程度上独立于皮层控制。
