Pericontusion axon sprouting is spatially and temporally consistent with a growth-permissive environment after traumatic brain injury.
Pericontusion axon sprouting is spatially and temporally consistent with a growth-permissive environment after traumatic brain injury.
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DOI：
10.1097/nen.0b013e3181cb5bee
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发表时间：
2010-02
影响因子：
3.2
通讯作者：
Sutton RL
中科院分区：
文献类型：
--
作者：
Harris NG;Mironova YA;Hovda DA;Sutton RL
We previously reported that pericontusional, extracellular chondroitin sulphate proteoglycans (CSPGs) are profoundly reduced for 3 weeks after experimental traumatic brain injury (TBI) indicating a potential growth-permissive window for plasticity. Here, we investigate the extracellular environment of sprouting neurons after controlled cortical impact injury in adult rats to determine the spatial and temporal arrangement of inhibitory and growth-promoting molecules in relation to growth-associated-protein 43-positive (GAP43+) neurons. Spontaneous cortical sprouting was maximal in pericontused regions at 7 and 14 days after injury but absent by 28 days. Perineuronal nets (PNNs) containing CSPGs were reduced at 7 days after injury in the pericontused region (p < 0.05), which was commensurate with a reduction in extracellular CSPGs. Sprouting was restricted to the PNNs and CSPG-deficient regions at 7 days, indicating that the pericontused region is temporarily and spatially permissive to new growth. At this time point, GAP43+ neurons were associated with brain regions containing cells positive for poly-sialic acid neural cell adhesion molecule but not with fibronectin-positive cells. Brain-derived neurotrophic factor was reduced in the immediate pericontused region at 7 days. Along with prior Western blot evidence, these data suggest that a lowered intrinsic growth stimulus together with a later return of growth-inhibitory CSPGs may contribute to the ultimate disappearance of sprouting neurons after TBI.
