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Rearrangement of the retino‐collicular projection after partial optic nerve crush in the adult rat
Author(s) -
Kreutz Michael R.,
Weise Jens,
Dieterich Daniela C.,
Kreutz Martin,
Balczarek Peter,
Böckers Tobias M.,
Wittkowski Werner,
Gundelfinger Eckart D.,
Sabel Bernhard A.
Publication year - 2004
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2004.03087.x
Subject(s) - optic nerve , superior colliculus , projection (relational algebra) , neuroscience , crush injury , anatomy , biology , medicine , computer science , surgery , algorithm
The establishment of retino‐collicular topography is a well‐investigated model of axon pathfinding and it was believed that this topography is irreversibly fixed throughout life. We now report that, after partial crush of the adult rat optic nerve, the anterograde transport of intravitreally‐injected tracers via axons of surviving retinal ganglion cells (RGC) in all retinal quadrants is confined to the rostro‐medial part of the superior colliculus (SC). This indicates that the retino‐collicular topography is rearranged after partial crush of the adult rat optic nerve. The reorganization starts in the injured optic nerve where surviving axonal fibres are demyelinized and bundled in the periphery of the optic nerve distal to the crush site. This is followed by a displacement of surviving axons to the medial part of the optic tract (OT) within 2 weeks. The infiltration of macrophages with the subsequent production of tumour necrosis factor‐α at the lesion site is a prerequisite for the altered retino‐collicular projection as blockade of tumour necrosis factor‐α signalling with the neutralizing antibody Infliximab abolishes reorganization in the SC and lateralization of RGC axons in the optic nerve and OT. This suggests that optic nerve inflammation is necessary for a progressive bundling of surviving RGC axons, probably via clearance of cellular debris which, in turn, may lead to a redistribution of RGC axons to the medial OT and rostro‐medial SC.