Author:

Abstract:

Induction of binocular central retinal lesions in adult cat abolishes visual activation of neurons in the corresponding region of primary visual cortex. Consequently, the sensory-deprived cortex undergoes topographic reorganization resulting in the restoration of visually driven activity. The aim of our study was to identify genes involved in adult cortical plasticity. Differential display on deprived and adjacent normal visual cortex, three days post-lesion, yielded several potential differentially expressed genes. One candidate gene was identified as Cu, Zn superoxide dismutase (SOD1). SOD1, an antioxidant enzyme present in cytoplasm of neurons and glia, has been implicated in plasticity processes such as sprouting and LTP (Shefner et al., 1999; Klann & Thiels , 1999). Differential display showed a higher SOD1 expression in deprived versus normal visual cortex as confirmed by semi-quantitative PCR. SQ PCR was performed on total RNA from deprived (central) and normal (peripheral) visual cortex of retinal lesion cats and from the corresponding cortical regions of control animals. Glyceraldehyde triphosphate dehydrogenase was used as reference gene to exclude possible differences due to unequal cDNA start concentrations. Normal animals exhibited either equal or higher SOD1 mRNA levels in peripheral cortex. However, in retinal lesion cat SOD1 expression was significantly higher (p<0.05) in central, deprived cortex compared to peripheral control cortex. These results suggest a role for SOD1 in neuronal activity and/or cortical plasticity.