Journal
BRAIN
Volume 135, Issue -, Pages 1210-1223Publisher
OXFORD UNIV PRESS
DOI: 10.1093/brain/aws027
Keywords
stroke; chondroitin sulphate proteoglycans; plasticity; ageing; perineuronal nets
Categories
Funding
- Medical Research Council [G0600998]
- Research Councils UK
- British Pharmacological Society (BPS)
- Capacity Building Award in Integrative Mammalian Biology
- Biotechnology and Biological Sciences Research Council
- Higher Education Funding Council for England
- Knowledge Transfer Partnerships
- Scottish Funding Council
- Biotechnology and Biological Sciences Research Council [BB/E527098/1] Funding Source: researchfish
- Medical Research Council [G0600998] Funding Source: researchfish
- BBSRC [BB/E527098/1] Funding Source: UKRI
- MRC [G0600998] Funding Source: UKRI
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Stroke is the dominant cause of sensorimotor disability that primarily affects the elderly. We now show that neuroplasticity and functional recovery after stroke is constrained by inhibitory chondroitin sulphates. In two blinded, randomized preclinical trials, degradation of chondroitin sulphate using chondroitinase ABC reactivated neuroplasticity and promoted sensorimotor recovery after stroke in elderly rats. Three days after stroke, chondroitinase ABC was microinjected into the cervical spinal cord to induce localized plasticity of forelimb sensorimotor spinal circuitry. Chondroitinase ABC effectively removed chondroitin sulphate from the extracellular matrix and perineuronal nets. Three different tests of sensorimotor function showed that chondroitinase ABC promoted recovery of forelimb function. Anterograde and retrograde tracing showed that chondroitinase ABC also induced sprouting of the contralesional corticospinal tract in the aged treated hemicord. Chondroitinase ABC did not neuroprotect the peri-infarct region. We show for the first time delayed chondroitinase ABC treatment promotes neuroanatomical and functional recovery after focal ischaemic stroke in an elderly nervous system.
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