Molecular control of brain plasticity and repair
Abstract
Recovery of function after damage to the CNS is limited due to the absence of axon regeneration and relatively low levels of plasticity. Plasticity in the CNS can be reactivated in the adult CNS by treatment with chondroitinase ABC, which removes glycosaminoglycan (GAG) chains from chondroitin sulfate proteoglycans (CSPGs). Plasticity in the adult CNS is restricted by perineuronal nets (PNNs) around many neuronal cell bodies and dendrites, which appear at the closure of critical periods and contain several inhibitory CSPGs. Formation of these structures and the turning off of plasticity is triggered by impulse activity in neurons. Expression of a link protein by neurons is the event that triggers the formation of PNNs. Treatment with chondroitinase removes PNNs and other inhibitory influences in the damaged spinal cord and promotes sprouting of new connections. However, promoting plasticity by itself does not necessarily bring back useful behavior; this only happens when useful connections are stabilized and inappropriate connections removed, driven by behavior. Thus after rodent spinal cord injury, combining a daily rehabilitation treatment for skilled paw function with chondroitinase produces much greater recovery than either treatment alone. The rehabilitation must be specific for the behavior that is to be enhanced because non-specific rehabilitation improves locomotor behavior but not skilled paw function. Plasticity-enhancing treatments may therefore open up a window of opportunity for successful rehabilitation.
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PNNs divide the neuronal surface into multiple compartments that control the lateral diffusion of neurotransmitter receptors within the plasma membrane.
“Second, PNNs divide the neuronal surface into multiple compartments, which control the diffusion of neurotransmitter receptors laterally within the plasma membrane (Fawcett, 2009; Frischknecht et al., 2009).”
From Losing the sugar coating: Potential impact of perineuronal net abnormalities on interneurons in schizophrenia (2015) · cites this paper as Fawcett, 2009
In the mammalian brain, ECM composition and properties undergo a profound transformation during late postnatal development.
“In the mammalian brain, the composition and properties of the ECM undergo a profound transformation during late postnatal development (Fawcett, 2009; Gundelfinger et al., 2010; Lander et al., 1997).”
From Losing the sugar coating: Potential impact of perineuronal net abnormalities on interneurons in schizophrenia (2015) · cites this paper as Fawcett, 2009
A juvenile form of ECM supportive of neurogenesis, cell migration, axonal outgrowth, and synaptogenesis is substituted by an adult form that predominantly restricts plasticity.
“A juvenile form of ECM, supportive of neurogenesis, cell migration, axonal outgrowth and synaptogenesis, is substituted by an adult form, which predominantly restricts plasticity (Bandtlow and Zimmermann, 2000; Faissner et al., 2010; Fawcett, 2009; Galtrey and Fawcett, 2007).”
From Losing the sugar coating: Potential impact of perineuronal net abnormalities on interneurons in schizophrenia (2015) · cites this paper as Fawcett, 2009
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Chemistry and Function of Glycosaminoglycans in the Nervous System
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- Authors
- Fawcett, J.
- Affiliations
- University of Cambridge (GB)
- Corresponding author
- Fawcett, James
- ORCID
- Fawcett, James
- Venue
- Progress in Brain Research
- Publisher
- Elsevier
- Published
- 2009
- Volume
- 175
- Pages
- 501-509
- ISSN
- 0079-6123 (ISSN-L)
- OpenAlex
- W1597802523
- Cited by
- 105
- References
- 7
- Citations by year
- 2025: 3 · 2024: 2 · 2023: 2 · 2022: 1 · 2021: 4 · 2020: 5 · 2019: 3 · 2018: 6 · 2017: 2 · 2016: 4 · 2015: 12 · 2014: 8 · 2013: 15 · 2012: 17
- FWCI
- 13.24
- Type
- book chapter
- Language
- en
- Open access
- closed
- Locations
- Progress in brain research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Health Sciences › Medicine › Pathology and Forensic Medicine › Spinal Cord Injury Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Proteoglycans and glycosaminoglycans research
- Keywords
- neuroplasticity, CNS repair, chondroitinase ABC, perineuronal nets, chondroitin sulfate proteoglycans, glycosaminoglycans, spinal cord injury, axon regeneration, rehabilitation, locomotor recovery, critical period, link protein, functional recovery
- MeSH terms
- Animals, Brain, Brain Injuries, Humans, Nerve Regeneration, Neuronal Plasticity, Neurons, Recovery of Function
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