The Involvement of the Myelin-Associated Inhibitors and Their Receptors in CNS Plasticity and Injury

Boghdadi, Anthony G.; Teo, Leon; Bourne, James A.

doi:10.1007/s12035-017-0433-6

Cited by 47 publications

(39 citation statements)

References 172 publications

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“…Axon‐repulsive molecules at the injury site, such as chondroitin sulphate proteoglycans (CSPGs) (reviewed in Kwok et al , ), myelin‐derived molecules (reviewed in Alizadeh, Dyck & Karimi‐Abdolrezaee, ; Boghdadi, Teo & Bourne, ) and classical repulsive axon‐guidance molecules (reviewed in de Wit & Verhaagen, ; Giger, Hollis & Tuszynski, ; Hollis, ) have a broad range of functions. Here we highlight that most axon‐repulsive molecules initiate inactivation of integrins (see Fig.…”

Section: Integrins Become Inactivated At the Lesion Site After Centramentioning

confidence: 99%

Integrins promote axonal regeneration after injury of the nervous system

et al. 2018

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Integrins are cell surface receptors that form the link between extracellular matrix molecules of the cell environment and internal cell signalling and the cytoskeleton. They are involved in several processes, e.g. adhesion and migration during development and repair. This review focuses on the role of integrins in axonal regeneration. Integrins participate in spontaneous axonal regeneration in the peripheral nervous system through binding to various ligands that either inhibit or enhance their activation and signalling. Integrin biology is more complex in the central nervous system. Integrins receptors are transported into growing axons during development, but selective polarised transport of integrins limits the regenerative response in adult neurons. Manipulation of integrins and related molecules to control their activation state and localisation within axons is a promising route towards stimulating effective regeneration in the central nervous system.

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Section: Integrins Become Inactivated At the Lesion Site After Centramentioning

confidence: 99%

Integrins promote axonal regeneration after injury of the nervous system

et al. 2018

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“…As discussed, myelin contains several growth-inhibitory molecules that limit both plasticity and axonal regeneration in the injured mammalian CNS ( Table 1 ), several of which have been extensively reviewed elsewhere [ 34 , 96 , 97 ]. A number of strategies to counteract and neutralize the effects of MAIs starting with complete demyelination have shown improvements for axonal regeneration and functional recovery.…”

Section: Myelin In the Nervous Systemmentioning

confidence: 99%

The Extracellular Environment of the CNS: Influence on Plasticity, Sprouting, and Axonal Regeneration after Spinal Cord Injury

2018

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The extracellular environment of the central nervous system (CNS) becomes highly structured and organized as the nervous system matures. The extracellular space of the CNS along with its subdomains plays a crucial role in the function and stability of the CNS. In this review, we have focused on two components of the neuronal extracellular environment, which are important in regulating CNS plasticity including the extracellular matrix (ECM) and myelin. The ECM consists of chondroitin sulfate proteoglycans (CSPGs) and tenascins, which are organized into unique structures called perineuronal nets (PNNs). PNNs associate with the neuronal cell body and proximal dendrites of predominantly parvalbumin-positive interneurons, forming a robust lattice-like structure. These developmentally regulated structures are maintained in the adult CNS and enhance synaptic stability. After injury, however, CSPGs and tenascins contribute to the structure of the inhibitory glial scar, which actively prevents axonal regeneration. Myelin sheaths and mature adult oligodendrocytes, despite their important role in signal conduction in mature CNS axons, contribute to the inhibitory environment existing after injury. As such, unlike the peripheral nervous system, the CNS is unable to revert to a “developmental state” to aid neuronal repair. Modulation of these external factors, however, has been shown to promote growth, regeneration, and functional plasticity after injury. This review will highlight some of the factors that contribute to or prevent plasticity, sprouting, and axonal regeneration after spinal cord injury.

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“…Chemical removal of PNNs in the cortex restores plasticity to the level of the critical period (Pizzorusso et al, 2002;Sorg et al, 2016;Lensjo et al, 2017). The third marker was intracortical myelin, which is also associated with ending critical periods and reducing spine turnover and LTP in the cortex (Akbik et al, 2012;Schwab & Strittmatter, 2014;Boghdadi et al, 2017). The second group of markers, with presumed opposite expression, included the enzyme CaMKII, because of its key role in mediating LTP (Lisman et al, 2012;Colgan & Yasuda, 2014).…”

Section: Introductionmentioning

confidence: 99%

Mirror trends of plasticity and stability indicators in primate prefrontal cortex

García‐Cabezas

Joyce

John

et al. 2017

Eur J of Neuroscience

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Research on plasticity markers in the cerebral cortex has largely focused on their timing of expression and role in shaping circuits during critical and normal periods. By contrast, little attention has been focused on the spatial dimension of plasticity-stability across cortical areas. The rationale for this analysis is based on the systematic variation in cortical structure that parallels functional specialization and raises the possibility of varying levels of plasticity. Here we investigated in adult rhesus monkeys the expression of markers related to synaptic plasticity or stability in prefrontal limbic and eulaminate areas that vary in laminar structure. Our findings revealed that limbic areas are impoverished in three markers of stability: intracortical myelin, the lectin Wisteria floribunda agglutinin, which labels perineuronal nets, and parvalbumin, which is expressed in a class of strong inhibitory neurons. By contrast, prefrontal limbic areas were enriched in the enzyme calcium/calmodulin-dependent protein kinase II (CaMKII), known to enhance plasticity. Eulaminate areas have more elaborate laminar architecture than limbic areas and showed the opposite trend: they were enriched in markers of stability and had lower expression of the plasticity related marker CaMKII. The expression of glial fibrillary acidic protein (GFAP), a marker of activated astrocytes, was also higher in limbic areas, suggesting that cellular stress correlates with the rate of circuit reshaping. Elevated markers of plasticity may endow limbic areas with flexibility necessary for learning and memory within an affective context, but may also render them vulnerable to abnormal structural changes, as seen in neurologic and psychiatric diseases.

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The Involvement of the Myelin-Associated Inhibitors and Their Receptors in CNS Plasticity and Injury

Cited by 47 publications

References 172 publications

Integrins promote axonal regeneration after injury of the nervous system

Integrins promote axonal regeneration after injury of the nervous system

The Extracellular Environment of the CNS: Influence on Plasticity, Sprouting, and Axonal Regeneration after Spinal Cord Injury

Mirror trends of plasticity and stability indicators in primate prefrontal cortex

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