Enlargement of cortical vibrissa representation in the surround of an ischemic cortical lesion

It has been shown that cortical lesions are associated with an increase of excitability in surrounding brain regions, and with a downregulation of GABA(A) receptors. In the present study we investigated whether this increased excitability affects the cortical map of inputs represented in areas surrounding the lesioned brain area. Focal lesions with a diameter of 2-2.5 mm were induced photochemically in the hindlimb area at the border of the primary somatosensory cortex of the rat. One week after lesioning, the cortical representation of the B3 vibrissa was studied using 14C-deoxyglucose (DG) autoradiography. In all animals mechanical stimulation of the B3 vibrissa produced a column-shaped DG-labeling in the somatosensory cortex, corresponding to the B3-barrel with a maximum of the glucose uptake in layer IV. In control animals without cortical lesions (n=6), stimulation increased the glucose uptake rate by 50.8+/-10.5% in layer IV. In lesioned animals (n=6) maximum DG-uptake in layer IV (54.8+/-8.6%) did not differ significantly from that in controls. However, as compared to control animals, lesioned animals showed also increased glucose uptake within the activated column in layers II/II (51.+/-11.1%, lesioned animals; 31.8+/-11.2%, controls; P<0.05, lesioned vs. control) and V (47.5+/-5.8%, lesioned animals, 28.8+/-10.5%, controls; P<0.05, lesioned vs. control). The diameter of the metabolically activated B3-barrel area of layer IV was expanded from 461.8+/-77.6 microm in control animals to 785.5+/-103.6 microm; P<0.01) in lesioned animals. Lesioned animals also showed expansion of the activated area in layers II/III (890.4+/-134.8 microm, lesioned animals; 430.6+/-95.1 microm, controls; P<0.01) and layer V (1117.5+/-163.6 microm, lesioned animals; 648.7+/-114.1 microm, controls; P<0.01). The depth profile of the activation columns showed a maximum in layer IV in control animals, which was expanded towards layers II/III and layer V in lesioned animals. It is concluded that cortical lesions alter the representational area of neighboring afferent inputs through disinhibition or 'unmasking' of pre-existing silent or ineffectual intracortical synapses. The present observations raise the possibility that the brain supports recovery from lesions by decreasing GABAergic inhibition, thereby facilitating a remapping of the cortical representation in neighboring brain areas.