Changes in NMDA-receptor function in the first week following laser-induced lesions in rat visual cortex

• Published in: Cerebral cortex (New York, N.Y. 1991) Vol. 22; no. 10; pp. 2392 - 2403
• Main Authors: Yan, Li, Imbrosci, Barbara, Zhang, Weiyi, Neubacher, Ute, Hatt, Hans, Eysel, Ulf T, Mittmann, Thomas
• Format: Journal Article
• Language: English
• Published: United States 01-10-2012
• Subjects: Animals; Lasers; Neuronal Plasticity - radiation effects; Rats; Rats, Wistar; Receptors, N-Methyl-D-Aspartate - metabolism; Visual Cortex - injuries; Visual Cortex - physiopathology
• ISSN: 1047-3211; 1460-2199
• DOI: 10.1093/cercor/bhr318

Focal brain injuries are accompanied by processes of functional reorganization that partially compensate the functional loss. In a previous study, extracellular recordings at the border of a laser-induced lesion in the visual cortex of rats showed an enhanced synaptic plasticity, which was mediated by the activity of NR2B-contaning NMDA-receptors (NMDARs) shedding light on the potential cellular mechanisms underlying this reorganization. Given the potentially important contribution of NMDARs in processes of functional reorganization, in the present study, we used the same lesion model to further investigate lesion-induced changes in function and localization of NMDARs in the vicinity of the lesion. The most important finding was a lesion-mediated functional reexpression of nonpostsynaptic, but according to our data, presynaptic or peri-/extrasynaptic NMDARs (preNMDARs), which were undetectable in age-matched (>P21) sham-operated controls. Notably, preNMDARs were able to boost both spontaneous and evoked synaptic glutamatergic transmission. At the postsynaptic site, we also disclosed an increase in the decay time constant of NMDARs mediated currents, which was accompanied by a decreased NR2A/NR2B ratio, as revealed by Western blot analysis. All together these findings provide new insights into the role of NMDARs activity during processes of functional reorganization following a focal lesion in the cerebral cortex.