IMR Press / FBL / Volume 21 / Issue 7 / DOI: 10.2741/4460

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Review

Chondroitin sulfate and neuronal disorders

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1 Institute for Advanced Research, Nagoya University, Furo-cho, Nagoya 464-8601, Japan
2 Bioscience and Biotechnology Center, Nagoya University, Furo-cho, Nagoya 464-8601, Japan
3 Department of Biochemistry, Kobe Pharmaceutical University, 4-19-1 Motoyamakita-machi, Kobe 658-8558, Japan
Academic Editor:Shunji Tomatsu
Front. Biosci. (Landmark Ed) 2016, 21(7), 1330–1340;
Published: 1 June 2016
(This article belongs to the Special Issue Glycosaminoglycans and related disorders)

The brain extracellular matrix (ECM) is involved in several aspects of neuronal development, plasticity, and pathophysiology. Chondroitin sulfate proteoglycans (CSPGs), consisting of core proteins with covalently attached chondroitin sulfate (CS) chains, are essential components of the brain ECM. During late postnatal development, CSPGs condense around parvalbumin-expressing inhibitory neurons (PV-cells) and form lattice-like ECM structures called perineuronal nets (PNNs). Enzymatic or genetic manipulation of PNNs reactivates neuronal plasticity in the adult brain, probably by resetting the excitatory/inhibitory balance in neural networks. Recent studies have indicated that PNNs control PV-cell function by enhancing the accumulation of specific proteins at the cell surface and/or acting as neuroprotective shields against oxidative stress. Since dysfunction of PV-cells and remodeling of CSPGs are commonly observed in several disorders, including schizophrenia, Costello syndrome, Alzheimer’s disease, and epilepsy, modulation of PV-cell function by CSPGs may provide a novel strategy for these neuronal disorders. Here we review the potential roles of CSPGs as therapeutic targets for neuronal disorders, with particular focus on structural changes of CS chains under pathological conditions.

Chondroitin Sulfate
Perineuronal Nets
Parvalbumin-Expressing Inhibitory Neuron
Costello Syndrome
Alzheimer’s Disease
Oxidative Stress
Ocular Dominance Plasticity
Critical Period
Neuronal Activity-Regulated Pentraxin
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