Aging of the brain, sensorimotor, and cognitive processes.
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Biomedical subjects
Publications and source records attributed to Hubert R Dinse.
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Aged rats show a characteristic decline of the sensorimotor state, most strikingly expressed in an impairment of the hindlimbs leading to significantly reduced sensory stimulation on the hindpaw. We review recent studies using optical imaging and electrophysiological recordings to investigate the effects of aging on somatosensory cortex and to identify age-related changes in terms of degeneration or plastic adaptation. For the cortical hindpaw representation, reduction of map size, receptive field enlargement and reduced response strength were described. None of these changes were reported in the forepaw representation in the same individual, however, in both the fore-and hindpaw representations response latencies and cerebral blood flow were affected. Changes of latencies and blood flow are best explained by degeneration, but the regional and specific changes of maps, receptive fields and response strength by plastic phenomena arising from the reduced sensory inputs. While the degenerative changes are not modifiable by enriched environmental conditions or application of Ca(2+) blocker, the plastic changes were fully reversible under these conditions. We discuss the implications of these findings for cognitive functions at old age and possible treatments of age-related changes in human subjects.
We provide a description of a correlation of lipofuscin accumulation and expression of glial fibrillary acidic protein in the cerebral cortex of aged rats. Glial fibrillary acidic protein showed a complementary distribution pattern to perineuronal nets, visualized with Wisteria floribunda agglutinin. With progressing age (12-36 months), a strong increase of lipofuscin and gliosis occurred in functionally characterized cortical areas, whereas a concomitant, area-specific loss of perineuronal nets was found in the cortical somatosensory representation of the hindlimbs. In contrast to lipofuscin accumulation and increased gliosis, the loss of perineuronal nets and the reduction of non-phosphorylated neurofilament H were in part reduced or prevented by housing the animals under enriched environmental conditions between 33 and 36 months of age. Especially the reduction of astrocytosis by 20% which coincided with a reduction in the loss of extracellular matrix components involved in forming the glia-neuron-interface demonstrates, that the aging cortex retains its potential for functional plasticity.
Changes in the expression of the nitric oxide synthase isoforms (NOS) have been implicated in age-related neurodegeneration, although mechanisms responsible for specific differences such as reduced cognitive and motor functions are not well understood. Immunohistochemical examination of the age-dependent NOS-I and NOS-II expression in aging rats at 3, 12, 24, 36 months of age as well as in 36 months old rats who spent their last 3 months in an enriched environment, revealed a significant decrease in NOS-I expression with aging. In contrast, NOS-II increased at 36 months. Old rats kept under enriched environmental conditions, however, showed strongly reduced NOS-II expression. These results indicate that both NOS-I and II may contribute to age-related degenerative processes, but in contrast to NOS-I the age-dependent changes of NOS-II are reduced or even reversed by stimulating environmental conditions.