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Metaplasticity of horizontal connections in the vicinity of focal laser lesions in rat visual cortex

机译:大鼠视皮层局灶性激光损伤附近水平连接的可塑性

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摘要

Focal cortical injuries are accompanied by a reorganization of the adjacent neuronal networks. An increased synaptic plasticity has been suggested to mediate, at least in part, this functional reorganization. Previous studies showed an increased long-term potentiation (LTP) at synapses formed by ascending fibres projecting onto layers 2/3 pyramidal cells following lesions in rat visual cortex. This could be important to establish new functional connections within a vertical cortical column. Importantly, horizontal intracortical connections constitute an optimal substrate to mediate the functional reorganization across different cortical columns. However, so far little is known about their potential implication in the functional rewiring post-lesion. Here, we investigated possible alterations of synaptic plasticity of horizontal connections in layers 2/3 in an ‘ex vivo–in vitro’ model of focal laser lesion in rat visual cortex. LTP at these synapses was found to be enhanced post-lesion, whereas long-term depression (LTD) was impaired, revealing a metaplastic shift toward strengthening of these synapses. Furthermore, we disclosed a prolonged decay-time constant of NMDAR-dependent currents, which can contribute to the enhanced LTP. Taken together these data revealed that a laser lesion-induced focal damage of the visual cortex is accompanied by a facilitated potentiation of horizontal synaptic connections in the vicinity of the focal injury. This specific strengthening of synaptic plasticity at horizontal connections in layers 2/3 might be one important cellular mechanism to compensate focal injury-mediated dysfunction in the cerebral cortex.
机译:局灶性皮质损伤伴随着相邻神经元网络的重组。已经建议增加的突触可塑性至少部分地介导这种功能重组。先前的研究表明,在大鼠视皮层损伤后,通过突伸到2/3锥体细胞层上的纤维上升而形成的突触处的长期增强作用(LTP)增加。这对于在垂直皮质柱内建立新的功能连接可能很重要。重要的是,水平皮质内连接构成了一个最佳的底物,可以介导跨不同皮质柱的功能重组。但是,到目前为止,关于它们在病变后功能性重新布线中的潜在影响知之甚少。在这里,我们研究了大鼠视皮层局灶性激光损伤的“离体-体外”模型中2/3层水平连接突触可塑性的可能改变。发现这些突触处的LTP在病变后增强,而长期抑郁症(LTD)受损,表明向这些突触的增生转变。此外,我们公开了依赖于NMDAR的电流的延长的衰减时间常数,这可能有助于增强LTP。这些数据加在一起表明,激光损伤引起的视觉皮层局灶性损害伴随着局灶性损伤附近水平突触连接的增强。在2/3层中水平连接处突触可塑性的这种特定增强可能是补偿大脑皮层局灶性损伤介导的功能障碍的一种重要细胞机制。

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