Premium
Metaplasticity of horizontal connections in the vicinity of focal laser lesions in rat visual cortex
Author(s) -
Imbrosci B.,
Eysel U. T.,
Mittmann T.
Publication year - 2010
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2010.198192
Subject(s) - neuroscience , long term potentiation , lesion , visual cortex , neuroplasticity , metaplasticity , cortex (anatomy) , synaptic plasticity , plasticity , biology , anatomy , psychology , materials science , receptor , biochemistry , psychiatry , composite material
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.