| Literature DB >> 10888746 |
M A Kingsbury1, E R Graf, B L Finlay.
Abstract
Previous research has demonstrated that precise patterns of axonal connectivity often develop during a series of stages characterized by pathfinding, target recognition, and address selection. This last stage involves the focusing of projections to a precisely defined region within the target. Because thalamic projections begin to innervate cortex before the latter stages are reached, these projections may be important in the establishment of adult-like patterns of cortical connectivity. To address this issue, we examined the mature corticopontine and corticospinal projections of visual cortex deprived of early thalamic input by visual thalamic ablation. Although ablations on the day of birth in hamsters did not disrupt the targeting of appropriate subcortical structures by visual cortical axons, they did alter the organization of projections within the basilar pons and spinal cord. The density and spread of visual corticopontine connections in lesioned animals was greatly increased relative to unlesioned animals, suggesting that thalamic afferents are required during address selection, when the topographic specificity of projections is established. To determine whether early visual thalamic ablation increases connectivity by stabilizing an exuberant developmental projection, we examined the normal development of visual corticopontine connections in hamsters ages postnatal days 1-17 (P1-P17). From the earliest ages, visual cortical axons innervate the pontine nucleus in regions specific to their adult projection zones and show progressive growth within these zones. At no time during development do projections exist that are equivalent to the projections found after thalamic ablation, suggesting that removal of thalamic input does not simply stabilize a developmental projection. Copyright 2000 Wiley-Liss, Inc.Entities:
Mesh:
Year: 2000 PMID: 10888746 DOI: 10.1002/1096-9861(20000814)424:1<165::aid-cne12>3.0.co;2-u
Source DB: PubMed Journal: J Comp Neurol ISSN: 0021-9967 Impact factor: 3.215