Effects of aging and sensory loss on glial cells in mouse visual and auditory cortices

被引:247
作者
Tremblay, Marie-Eve [1 ,2 ]
Zettel, Martha L. [1 ,2 ]
Ison, James R. [1 ,2 ,3 ]
Allen, Paul D. [1 ,2 ]
Majewska, Ania K. [1 ,2 ]
机构
[1] Univ Rochester, Dept Neurobiol & Anat, Rochester, NY 14642 USA
[2] Univ Rochester, Ctr Visual Sci, Rochester, NY 14642 USA
[3] Univ Rochester, Dept Brain & Cognit Sci, Rochester, NY USA
基金
加拿大健康研究院;
关键词
microglia; oligodendrocyte; morphology; phagocytosis; CBA; CaJ; C57BL; 6J; AGE-RELATED-CHANGES; MONKEY CEREBRAL-CORTEX; LONG-TERM POTENTIATION; INFERIOR COLLICULUS; NEUROGLIAL CELLS; CREB PHOSPHORYLATION; COGNITIVE DECLINE; MICROGLIAL CELLS; CALBINDIN D-28K; NERVOUS-SYSTEM;
D O I
10.1002/glia.22287
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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. (c) 2012 Wiley Periodicals, Inc.
引用
收藏
页码:541 / 558
页数:18
相关论文
共 107 条
[1]   Apoptosis of retrogradely degenerating neurons occurs in association with the accumulation of perikaryal mitochondria and oxidative damage to the nucleus [J].
Al-Abdulla, NA ;
Martin, LJ .
AMERICAN JOURNAL OF PATHOLOGY, 1998, 153 (02) :447-456
[2]   THE EFFECT OF ADVANCED OLD-AGE ON THE NEURON CONTENT OF THE CEREBRAL-CORTEX - OBSERVATIONS WITH AN AUTOMATIC IMAGE ANALYZER POINT COUNTING METHOD [J].
ANDERSON, JM ;
HUBBARD, BM ;
COGHILL, GR ;
SLIDDERS, W .
JOURNAL OF THE NEUROLOGICAL SCIENCES, 1983, 58 (02) :235-246
[3]   THE TEMPORAL EVOLUTION OF HYPOGLYCEMIC BRAIN-DAMAGE .1. LIGHT-MICROSCOPIC AND ELECTRON-MICROSCOPIC FINDINGS IN THE RAT CEREBRAL-CORTEX [J].
AUER, RN ;
KALIMO, H ;
OLSSON, Y ;
SIESJO, BK .
ACTA NEUROPATHOLOGICA, 1985, 67 (1-2) :13-24
[4]   Age-related defects in spatial memory are correlated with defects in the late phase of hippocampal long-term potentiation in vitro and are attenuated by drugs that enhance the cAMP signaling pathway [J].
Bach, ME ;
Barad, M ;
Son, H ;
Zhuo, M ;
Lu, YF ;
Shih, R ;
Mansuy, I ;
Hawkins, RD ;
Kandel, ER .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (09) :5280-5285
[5]   REGION-SPECIFIC AGE EFFECTS ON AMPA SENSITIVITY - ELECTROPHYSIOLOGICAL EVIDENCE FOR LOSS OF SYNAPTIC CONTACTS IN HIPPOCAMPAL FIELD CA1 [J].
BARNES, CA ;
RAO, G ;
FOSTER, TC ;
MCNAUGHTON, BL .
HIPPOCAMPUS, 1992, 2 (04) :457-468
[6]   PHYSIOLOGICAL COMPENSATION FOR LOSS OF AFFERENT SYNAPSES IN RAT HIPPOCAMPAL GRANULE CELLS DURING SENESCENCE [J].
BARNES, CA ;
MCNAUGHTON, BL .
JOURNAL OF PHYSIOLOGY-LONDON, 1980, 309 (DEC) :473-485
[7]   LTP induction threshold change in old rats at the perforant path-granule cell synapse [J].
Barnes, CA ;
Rao, G ;
Houston, FP .
NEUROBIOLOGY OF AGING, 2000, 21 (05) :613-620
[8]   Early-life infection is a vulnerability factor for aging-related glial alterations and cognitive decline [J].
Bilbo, Staci D. .
NEUROBIOLOGY OF LEARNING AND MEMORY, 2010, 94 (01) :57-64
[9]   Immune signalling in neural development, synaptic plasticity and disease [J].
Boulanger, LM ;
Shatz, CJ .
NATURE REVIEWS NEUROSCIENCE, 2004, 5 (07) :521-531
[10]   The mitochondrial-lysosomal axis theory of aging - Accumulation of damaged mitochondria as a result of imperfect autophagocytosis [J].
Brunk, UT ;
Terman, A .
EUROPEAN JOURNAL OF BIOCHEMISTRY, 2002, 269 (08) :1996-2002