Marie-Ève Tremblay and Martha L. Zettel contributed equally to this work.
Effects of aging and sensory loss on glial cells in mouse visual and auditory cortices
Article first published online: 5 JAN 2012
Copyright © 2012 Wiley Periodicals, Inc.
Volume 60, Issue 4, pages 541–558, April 2012
How to Cite
Tremblay, M.-È., Zettel, M. L., Ison, J. R., Allen, P. D. and Majewska, A. K. (2012), Effects of aging and sensory loss on glial cells in mouse visual and auditory cortices. Glia, 60: 541–558. doi: 10.1002/glia.22287
- Issue published online: 8 FEB 2012
- Article first published online: 5 JAN 2012
- Manuscript Accepted: 5 DEC 2011
- Manuscript Received: 27 OCT 2011
- Whitehall Foundation
- Alfred P. Sloan Foundation
- Burroughs Wellcome Fund (a Career Award in the Biomedical Sciences. Grant Number: EY019277
- NIH-NIA Research. Grant Number: AG09534
- NIDCD (NIH Center). Grant Number: P30 DC05409
- NEI. Grant Number: P30 EY01319
- Schmitt Program for Integrative Brain Research
- Fonds de la Recherche en Santé du Québec (FRSQ)
- Canadian Institutes of Health Research (CIHR)
- Postdoctoral Fellowships
Normal aging is often accompanied by a progressive loss of receptor sensitivity in hearing and vision, whose consequences on cellular function in cortical sensory areas have remained largely unknown. By examining the primary auditory (A1) and visual (V1) cortices in two inbred strains of mice undergoing either age-related loss of audition (C57BL/6J) or vision (CBA/CaJ), we were able to describe cellular and subcellular changes that were associated with normal aging (occurring in A1 and V1 of both strains) or specifically with age-related sensory loss (only in A1 of C57BL/6J or V1 of CBA/CaJ), using immunocytochemical electron microscopy and light microscopy. While the changes were subtle in neurons, glial cells and especially microglia were transformed in aged animals. Microglia became more numerous and irregularly distributed, displayed more variable cell body and process morphologies, occupied smaller territories, and accumulated phagocytic inclusions that often displayed ultrastructural features of synaptic elements. Additionally, evidence of myelination defects were observed, and aged oligodendrocytes became more numerous and were more often encountered in contiguous pairs. Most of these effects were profoundly exacerbated by age-related sensory loss. Together, our results suggest that the age-related alteration of glial cells in sensory cortical areas can be accelerated by activity-driven central mechanisms that result from an age-related loss of peripheral sensitivity. In light of our observations, these age-related changes in sensory function should be considered when investigating cellular, cortical, and behavioral functions throughout the lifespan in these commonly used C57BL/6J and CBA/CaJ mouse models. © 2012 Wiley Periodicals, Inc.