αB-CRYSTALLIN, which is abundantly expressed in the lens but also in a diversity of other tissues, functions as a stress-inducible molecular chaperone and is increased in brain neurodegenerative diseases. We compared retinal αB-crystallin expression in a model of inherited retinal degeneration, th erdmouse, and controls. Northern andin sit uhybridization analysis showe αB-crystallin mRNA to have an altered spatio-temporal pattern with increased levels localized to glial cells in the degenerative state. Immunocytochemistry confirmed increased expression at Müller cells and astrocytes, together with transiently increased localization to the degenerating photoreceptors. These findings suggest that increase dαB-crystallin expression is associated with glial cell reaction to neuronal damage in the retina, and may comprise part of the retina's overall defensive response to the stress of apoptotic photoreceptor cell death.