ArticleThe Journal of physiology2010
Metaplasticity of horizontal connections in the vicinity of focal laser lesions in rat visual cortex.
Article in The Journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Traumatic brain injury to primary visual cortex produces long-lasting circuit dysfunction.Communications biology · 2021Article
- Adult cortical plasticity following injury: Recapitulation of critical period mechanisms?Neuroscience · 2014Review
- Shift from phasic to tonic GABAergic transmission following laser-lesions in the rat visual cortex.Pflugers Archiv : European journal of physiology · 2013Article
- A simple rule for dendritic spine and axonal bouton formation can account for cortical reorganization after focal retinal lesions.PLoS computational biology · 2013Article
- Functional consequences of the disturbances in the GABA-mediated inhibition induced by injuries in the cerebral cortex.Neural plasticity · 2011Review
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Authors and funding
3 authors.
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Abstract
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.
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