Neuronal mechanisms underlying transhemispheric diaschisis following focal cortical injuries

Neuronal mechanisms underlying transhemispheric diaschisis following focal cortical injuries
复制标题

DOI:
10.1007/s00429-014-0750-8
复制
发表时间:
2015-05-01
影响因子:
3.1
通讯作者:
Mittmann, Thomas
Mittmann, Thomas
中科院分区:
医学3区
文献类型:
--
作者:
Imbrosci, Barbara;Ytebrouck, Ellen;Mittmann, Thomas

文献摘要

被引文献

相似文献

单侧皮质损伤引起的干扰通常扩散到损伤对侧的半球。这种影响对侧皮层的功能改变被称为跨半球神经功能联系不能,被认为是导致神经功能缺损和损伤后功能重组的原因。尽管对恢复有着深远的影响,但人们对这种现象背后的细胞机制知之甚少。在本研究中,transemispheric神经联系不能进行了研究,在体内离体模型的单侧病变,诱导的红外激光在大鼠视皮层。通过细胞活性标记物zif 268的表达水平评估视觉诱发的皮质活性,其显示病变对侧皮质的升高。在体外膜片钳记录从第2/3层锥体神经元的兴奋性,抑制性平衡的变化有利于兴奋性,特别是在未受损的半球。第5层的主要神经元表现出增加的自发放电率对侧的病变,而受伤的皮层细胞显示减少体电流注入后的放电。这些数据表明,皮层损伤触发了损伤对侧半球神经元活动的增强。我们的研究结果构成了在细胞水平上理解跨半球神经功能障碍的重要一步。
Unilateral cortical lesions cause disturbances often spreading into the hemisphere contralateral to the injury. The functional alteration affecting the contralesional cortex is called transhemispheric diaschisis and is believed to contribute to neurological deficits and to processes of functional reorganization post-lesion. Despite the profound implications for recovery, little is known about the cellular mechanisms that underlie this phenomenon. In the present study, transhemispheric diaschisis was investigated with an in vivo-ex vivo model of unilateral lesions, induced by an infrared laser in rat visual cortex. Visually evoked cortical activity was evaluated by the expression level of the cellular activity marker zif268, which showed an elevation in the cortex contralateral to the lesion. In vitro patch-clamp recordings from layer 2/3 pyramidal neurons revealed a shift in the excitatory-inhibitory balance in favor of excitability, particularly expressed in the undamaged hemisphere. Layer 5 principal neurons displayed an increased spontaneous firing rate contralateral to the lesion, while cells of the injured cortex displayed a reduced firing upon somatic current injection. These data suggest that a cortical lesion triggers an enhanced neuronal activity in the hemisphere contralateral to the damage. Our findings constitute an important step toward the understanding of transhemispheric diaschisis on the cellular level.