ISSN:
1432-0878
Keywords:
Cerebral cortex
;
Associational connections
;
Synaptogenesis, reactive
;
Neuroplasticity
;
6-OHDA
Source:
Springer Online Journal Archives 1860-2000
Topics:
Biology
,
Medicine
Notes:
Summary Neuroplastic changes in associational connections were investigated 3 weeks after the intrinsic organization of the visual cortex of rats had been partially damaged by small cylindrical lesions (type I). These lesions caused the degeneration of short intracortical connections and associational connections that form patches in the primary and secondary visual areas. The resulting terminal degeneration disappeared within 20 days p.o. after which only some fiber degeneration was evident in the infragranular layers. Patches of terminal degeneration reappeared in the vicinity of the stab wounds, when the associational connections between the retrosplenial and the primary visual cortex had been secondarily interrupted by elongated lesions (type II), which penetrated the paramedian cortex and subcortical white matter. When type-II lesions were made in the intact cortex, patches of degeneration were absent, although in both cases some terminal degeneration was diffusely distributed in the primary visual cortex. Horseradish peroxidase (HRP) was applied to sites similar to those where type-I lesions were applied. In the intact cortex, HRP caused a granular labeling of numerous neurons in various positions including the retrosplenial cortex and patches of the postero-median visual cortex. HRP was also applied to type-I lesions that had been made 3 weeks earlier. In these cases, apparently HRP labeled the same subpopulations of neurons as it did in the intact cortex. However, a fraction of the labeled neurons showed a Golgilike staining (e.g., 27% of the labeled neurons in the retrosplenial cortex) only when HRP was applied to stab wounds. These results suggest that the breakdown of corticocortical connections in foci of the primary visual cortex causes a focal augmentation of specific associational connections, which are weak and diffusely distributed in the intact adult cortex of rats. Re-innervation originates from subpopulations of associative neurons in the retrosplenial and postero-median visual cortex. Preliminary experiments indicate that the failure of neonatal treatment with 6-OHDA to suppress this lesion-induced plasticity is not dependent on an intact noradrenergic innervation.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00214548
Permalink
