Lesion-induced enhancement of LTP in rat visual cortex is mediated by NMDA receptors containing the NR2B subunit.

There is emerging evidence that injury of the cerebral cortex is followed by processes of enhanced neuroplasticity. In the present study, we investigate the functional properties of NMDA receptors (NMDARs) in the surround of focal lesions with recordings of extracellular field potentials (FPs) in acute slices of rat visual cortex at survival times of 2-6 days. FPs were recorded in cortical layer III lateral to the lesion, while long-term potentiation (LTP) was induced by theta-burst stimulation (TBS) in layer IV. The predominantly AMPA receptor-mediated FPs displayed a significantly enhanced LTP in the surround of the lesion at distances of 2-3.2 mm. The LTP was completely blocked by the NMDAR antagonist D-AP5. Ifenprodil, an antagonist of NMDARs containing the NR2B subunit, only slightly affected the LTP in slices from sham-operated animals, but significantly reduced the LTP in slices from lesioned rats. We quantitatively analysed the proportion of NMDARs containing the NR2B subunit after lesions by applying ifenprodil to pharmacologically isolated NMDAR-FPs. The NR2B antagonist reduced the NMDAR-FPs significantly more strongly at distances of 2.0-3.2 mm from the border of the lesion. This indicates that the early phase of increased synaptic long-term plasticity in the surround of cortical lesions is accompanied by an up-regulation of NMDARs containing the NR2B subunit.