Focal lesions in the visual cortex have been shown to induce enlarged receptive field sizes and an enhanced long-term potentiation (LTP). However, the synaptic mechanism of the lesion-induced facilitation of LTP is not fully understood. Therefore, the
present thesis studied possible changes in pre- and postsynaptic function of neurons located at the border of lesion in rat visual cortex. This study showed an increased presynaptic glutamate release probability in lesion-treated visual cortex. The
enhanced presynaptic glutamate release is mediated by activation of the presynaptic NMDARs and BDNF-TrkB receptor pathway. The lesion also affects the functional properties of postsynaptically located NMDARs containing the NR2B subunits. In addition,
neurons at the border of the injury showed a decreased GABAergic inhibition. The findings of the present study indicate that a focal cortical lesion in visual cortex changes both, the pre- and postsynaptic function of neighbouring neurons.