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Reduction in CNS scar formation without concomitant increase in axon regeneration following treatment of adult rat brain with a combination of antibodies to TGFβ 1 and β 2
Author(s) -
Moon L. D. F.,
Fawcett J. W.
Publication year - 2001
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.0953-816x.2001.01795.x
Subject(s) - microglia , glial fibrillary acidic protein , dopaminergic , gliosis , axon , glial scar , regeneration (biology) , pathology , transforming growth factor , astrogliosis , medicine , biology , astrocyte , inflammation , dopamine , endocrinology , central nervous system , immunohistochemistry , anatomy , immunology , microbiology and biotechnology
In this study we investigated whether CNS axons regenerate following attenuation of scar formation using a combination of antibodies against two isoforms of transforming growth factor beta (TGFβ). Anaesthetized adult rats were given unilateral mechanical lesions of the nigrostriatal tract. Implantation of transcranial cannulae allowed wounds to be treated with a combination of antibodies against TGFβ 1 and TGFβ 2 once daily for 10 days postaxotomy. Eleven days post‐transection brains from animals under terminal anaesthesia were recovered for histological evaluation. Gliosis, inflammation and the response of dopaminergic nigral axons were assessed by immunolabelling. Treatment with antibodies against TGFβ 1 and TGFβ 2 attenuated (but did not abolish) the response of glial fibrillary acidic protein (GFAP)‐immunoreactive astrocytes and of NG2‐immunoreactive glia but did not attenuate the response of CR3‐immunoreactive microglia and macrophages. However, this reduction in scar formation was not accompanied by growth of cut dopaminergic nigral axons. We conclude that treatment of injured adult rat brain with a combination of antibodies against TGFβ 1 and TGFβ 2 results in a reduction of scar formation but that this is not sufficient to enhance spontaneous long distance CNS axon regeneration.