Annual Meeting of the Society for Neuroscience, Date: 2007/11/03 - 2007/11/07, Location: San Diego (USA)

Publication date: 2007-11-03

Author:

Hu, Tjing-Tjing
Cnops, Lieselotte ; Van den Bergh, Gert ; Heylen, Kevin ; Eysel, Ulf T ; Arckens, Lut

Abstract:

Small centrally placed lesions in both retinas lead to loss of visual input in the central visual cortex of the adult cat. As a consequence, a topographical reorganization occurs within this sensory-deprived cortical lesion projection zone (LPZ) as measured by electrophysiology. This recovery coincides with changes in activity balance and gene expression. We investigated these modifications in function of post-lesion survival time (14 days to 8 months) in three regions in primary visual area 17: the most centrally situated permanent LPZ (LPZp), the far peripheral intact projection zone (IPZ) and the border zone between the LPZ and the IPZ, the transient LPZ (LPZt). Firstly, we quantified differences in neuronal activity by means of real-time PCR for the well-known activity marker c-fos in the LPZp, LPZt and IPZ of area 17. The central retinal lesions induced an activity decrease not only in the central LPZp and LPZt, but also outside the LPZ in the peripheral IPZ in the first weeks post-lesion. With time however, the LPZt and the IPZ exhibited a clear recovery of the c-fos expression and thus of neuronal activity. Secondly, we analysed protein expression patterns in controls and retinal lesion cats with 2-dimensional differential gel electrophoresis to identify differentially expressed proteins, which might have a role in brain plasticity. With this study we have traced 75 differential spots for the three regions in area 17. Area 17 showed clear region-specific protein expression changes. Even the protein expression in the peripheral IPZ differed from the corresponding cortical zone of normal subjects. We conclude that alterations in activity balance and protein expression in the central LPZp and LPZt as well as in the peripheral IPZ have an important role in the processes that mediate lesion-induced cortical plasticity.