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Topical glucocorticoids modulate the lesion interface after cerebral cortical stab wounds in adult rats.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Li, Mingzhou David, Samuel Paul |
| Copyright Year | 1996 |
| Abstract | A lesion interface, consisting of a glia limitans lined by a laminin-rich basal lamina and leptomeningeal cells, forms within 2-3 weeks after penetrating wounds to the adult mammalian central nervous system (CNS). This interface prevents the growth of axons across the lesion. We have examined the effects of topically applied steroids on the formation of such an interface after stab wounds to the adult rat cerebral cortex. Immediately after lesioning, the surface of cortex in the region of the wound was treated with a topical application of either 0.1% halcinonide or 0.05% betamethasone dipropionate or their respective placebos. Cryostat sections through the lesioned area were obtained 3 weeks later and assessed by immunofluorescence. Steroid treatment attenuated all components of the lesion. The continuous anti-laminin labeling along the lesion in untreated rats became patchy after steroid treatment. The number of leptomeningeal cells that infiltrated into the wound was reduced in the laminin-negative regions in steroid-treated rats. In addition, astrocytic processes in the laminin-negative regions after steroid treatment were loosely arranged, compared with the tightly packed parallel processes forming the glia limitans in laminin-positive regions in controls. The mechanism of steroid-mediated attenuation of the lesion interface was examined in vitro. Betamethasone but not halcinonide reduced laminin secretion slightly in leptomeningeal cell cultures, but both steroids reduced cell proliferation. These results suggest that steroids modulate the formation of the lesion interface after CNS injury, at least in part by decreasing leptomeningeal cell proliferation. Such modulation of the lesion interface by steroids or other agents may permit the growth of axons across the lesion site and thus could enhance the overall degree of axon regeneration if other factors such as neurotrophic support and neutralization of axon growth inhibitory molecules are optimized. |
| Starting Page | 044317 |
| Ending Page | 044317 |
| Page Count | 1 |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://www.nlc-bnc.ca/obj/s4/f2/dsk2/ftp01/MQ37140.pdf |
| PubMed reference number | 8972799v1 |
| Volume Number | 18 |
| Issue Number | 4 |
| Journal | Glia |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | Adrenal Cortex Application Program Interface Basal lamina CNS disorder Cell Culture Techniques Cell Proliferation Cerebral cortex Cryostat Halcinonide Head Injuries, Penetrating Infiltration Laminin Leptomeninges Mammals Natural regeneration Neuroglia Neutralization (Chemistry) Phase II/III Trial Placebos Steroid therapy Steroids Wounds, Stab axon regeneration betamethasone dipropionate childhood central nervous system germ cell tumor |
| Content Type | Text |
| Resource Type | Article |
