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Publication : Cortical and subcortical projections to primary visual cortex in anophthalmic, enucleated and sighted mice.

First Author  Charbonneau V Year  2012
Journal  Eur J Neurosci Volume  36
Issue  7 Pages  2949-63
PubMed ID  22780435 Mgi Jnum  J:207654
Mgi Id  MGI:5559288 Doi  10.1111/j.1460-9568.2012.08215.x
Citation  Charbonneau V, et al. (2012) Cortical and subcortical projections to primary visual cortex in anophthalmic, enucleated and sighted mice. Eur J Neurosci 36(7):2949-63
abstractText  The purpose of this study was to identify and compare the afferent projections to the primary visual cortex in intact and enucleated C57BL/6 mice and in ZRDCT/An anophthalmic mice. Early loss of sensory-driven activity in blind subjects can lead to activations of the primary visual cortex by haptic or auditory stimuli. This intermodal activation following the onset of blindness is believed to arise through either unmasking of already present cortical connections, sprouting of novel cortical connections or enhancement of intermodal cortical connections. Studies in humans have similarly demonstrated heteromodal activation of visual cortex following relatively short periods of blindfolding. This suggests that the primary visual cortex in normal sighted subjects receives afferents, either from multisensory association cortices or from primary sensory cortices dedicated to other modalities. Here cortical afferents to the primary visual cortex were investigated to determine whether the visual cortex receives sensory input from other modalities, and whether differences exist in the quantity and/or the structure of projections found in sighted, enucleated and anophthalmic mice. This study demonstrates extensive direct connections between the primary visual cortex and auditory and somatosensory areas, as well as with motor and association cortices in all three animal groups. This suggests that information from different sensory modalities can be integrated at early cortical stages and that visual cortex activations following visual deprivations can partly be explained by already present intermodal corticocortical connections.
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