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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Alterations in GAP-43 and synapsin immunoreactivity provide evidence for synaptic reorganization in adult cat dorsal lateral geniculate nucleus following retinal lesions.

Growth-associated protein-43 (GAP-43) and synapsin were used as molecular markers for synaptic reorganization in the adult cat visual system following sensory deprivation. Small binocular retinal lesions (central 10 degrees) were made with a xenon light photocoagulator in adult cats. One, 3, 5 and 7 weeks after induction of the lesion, the neuropil levels of synapsin and GAP-43 in the dorsal lateral geniculate nucleus (dLGN) and area 17 were determined by immunocytochemistry. GAP-43 displayed a moderately low basal level in the dLGN of normal adult cats. The parvocellular C layers and the interlaminar plexi were characterized by higher immunoreactivity for GAP-43. Lesion-induced alterations were observed in all layers: GAP-43 immunoreactivity increased in the part of the dLGN representing central vision. This increase was maximal 3 weeks after the lesion. Under our experimental conditions, sensory deprivation did not significantly alter GAP-43 levels in the visual cortex. The changes in synapsin immunoreactivity were also restricted to the dLGN. In this nucleus, synapsin immunoreactivity decreased in all layers in the part subserving central vision 1 week after lesion. By 3 weeks after lesion, the level of synapsin had already returned to normal. This study provides evidence for a capacity for structural remodelling in primary sensory brain areas such as the dLGN throughout adult life. The observed changes in GAP-43 and synapsin in the dLGN suggest that synaptic reorganization is induced by retinal lesions. Normalization of synaptic density and activity could be important for the survival of the partially deafferented geniculate neurons.[1]


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