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Gigout, S.

Publications and source records attributed to Gigout, S..

2 recordsLinked to original sources

4-methylumbelliferone enhances neuroplasticity in the central nervous system: potential oral treatment for SCI

Perineuronal nets (PNNs) are specialised extracellular matrix (ECM) structures that act as key plasticity regulators to the central nervous system. Removal of PNNs using chondroitinase ABC injections restores plasticity, however, there are limitations to its application to due to its enzymatic nature. Here, we explore the use of a small molecule 4-methylumbelliferone (4-MU) as an alternative non-invasive strategy to reversibly remove PNNs and enhance plasticity. Oral administration of 4-MU for 10 days successfully and dynamically removed PNNs in vitro. While 4-MU, preferentially downregulated hyaluronan in the spinal cord, a down-regulation of chondroitin sulphate proteoglycans is also observed in the cortex. Long term administration for 8-weeks administration revealed a partial removal of PNNs, and that injury-induced mechanisms promoting cortical structural plasticity are linked to endogenous modulation of ECM molecules. 4-MU is a new tool to unravel the limits of normal and pathological PNN-mediated plasticity.

neuroscience↗

Restoring the pattern of perineuronal net sulphation corrects age-related memory loss

Memory loss is a usual consequence of ageing and aged mice show progressive deficits in memory tasks. In aged brains, perineuronal nets (PNNs), which are implicated in plasticity and memory, become inhibitory due to decreased 6-sulphation of their glycan chains (C6S). Removal of PNNs or digestion of their glycosaminoglycans rescued age-related memory loss. Premature reduction of permissive C6S by transgenic deletion of chondroitin 6-sulfotransferase led to very early memory loss. However, restoring C6S levels in aged animals by AAV delivery or transgenic expression of 6-sulfotransferase restored memory. Low C6S levels caused loss of cortical long-term potentiation, which was restored by AAV-mediated 6-sulfotransferase delivery. The study shows that loss of C6S in the aged brain leads to declining memory and cognition. Age-related memory impairment was restored by C6S replacement or other interventions targeting perineuronal nets

neuroscience↗