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大鼠额叶皮质微小光血栓形成性损伤后的扩展性脑去抑制

Extended brain disinhibition following small photothrombotic lesions in rat frontal cortex.

作者信息

Buchkremer-Ratzmann I, Witte O W

机构信息

Neurologische Klinik, Heinrich-Heine Universität, Düsseldorf, Germany.

出版信息

Neuroreport. 1997 Jan 20;8(2):519-22. doi: 10.1097/00001756-199701200-00028.

Abstract

The effect of an ischaemic focal cortical lesion on the excitability of surrounding and remote brain areas was investigated. Infarcts were produced photothrombotically in rat frontal cortex and brain excitability was assessed by a extracellular paired-pulse stimulation in coronal slices 7 days later. The cortical lesions caused a reduction of inhibition. The extent and grade of these electrophysiological effects depended on the depth of the lesion: in animals with a lesion affecting the deeper cortical layers a pronounced transcortical diaschisis was found, whereas animals with a shallow lesion showed only a slight ipsilateral affliction. The study shows that focal lesions in the motor cortex cause widespread disinhibition, probably resulting from deafferentation, and these may have a significant impact on recovery of function.

摘要

研究了缺血性局灶性皮质损伤对周围和远处脑区兴奋性的影响。通过光血栓法在大鼠额叶皮质制造梗死灶,7天后在冠状切片中通过细胞外双脉冲刺激评估脑兴奋性。皮质损伤导致抑制作用减弱。这些电生理效应的程度和等级取决于损伤的深度:在损伤累及皮质深层的动物中发现明显的跨皮质失联络,而损伤较浅的动物仅表现出轻微的同侧受累。该研究表明,运动皮质的局灶性损伤会导致广泛的去抑制,这可能是由于传入神经阻滞引起的,并且这些可能对功能恢复产生重大影响。

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