Immunohistochemical mapping of perineuronal nets containing chondroitin unsulfate proteoglycan in the rat central nervous system

Bertolotto, Antonio; Manzardo, E.; Guglielmone, R

doi:10.1007/s004410050538

Cited by 70 publications

(70 citation statements)

References 44 publications

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“…Recent evidence suggests that ChABC administration into visual cortex combined with reverse lid suture stimulates sufficient plasticity to restore normal vision to the once deprived eye in animals made amblyopic at weaning (Pizzorusso et al, 2006). In the spinal cord, ChABC treatment likely affects this extracellular covering as well as scar-associated matrix, allowing the regenerating neurons to grow more vigorously toward and make indirect or direct connections with denervated motoneurons (Bertolotto et al, 1996;Takahashi-Iwanaga et al, 1998;Murakami and Ohtsuka, 2003). It is conceivable that formation of new, functional synapses between the regenerating axons emerging from the PN graft and the target host neuronal populations may, in turn, allow an additional measure of plasticity from local circuitry or from contralateral descending fiber systems once the perineuronal net is degraded.…”

Section: Discussionmentioning

confidence: 99%

Combining an Autologous Peripheral Nervous System “Bridge” and Matrix Modification by Chondroitinase Allows Robust, Functional Regeneration beyond a Hemisection Lesion of the Adult Rat Spinal Cord

et al. 2006

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Chondroitinase-ABC (ChABC) was applied to a cervical level 5 (C5) dorsal quadrant aspiration cavity of the adult rat spinal cord to degrade the local accumulation of inhibitory chondroitin sulfate proteoglycans. The intent was to enhance the extension of regenerated axons from the distal end of a peripheral nerve (PN) graft back into the C5 spinal cord, having bypassed a hemisection lesion at C3. ChABC-treated rats showed (1) gradual improvement in the range of forelimb swing during locomotion, with some animals progressing to the point of raising their forelimb above the nose, (2) an enhanced ability to use the forelimb in a cylinder test, and (3) improvements in balance and weight bearing on a horizontal rope. Transection of the PN graft, which cuts through regenerated axons, greatly diminished these functional improvements. Axonal regrowth from the PN graft correlated well with the behavioral assessments. Thus, many more axons extended for much longer distances into the cord after ChABC treatment and bridge insertion compared with the control groups, in which axons regenerated into the PN graft but growth back into the spinal cord was extremely limited. These results demonstrate, for the first time, that modulation of extracellular matrix components after spinal cord injury promotes significant axonal regeneration beyond the distal end of a PN bridge back into the spinal cord and that regenerating axons can mediate the return of useful function of the affected limb.

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Section: Discussionmentioning

confidence: 99%

Combining an Autologous Peripheral Nervous System “Bridge” and Matrix Modification by Chondroitinase Allows Robust, Functional Regeneration beyond a Hemisection Lesion of the Adult Rat Spinal Cord

et al. 2006

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“…Fujita and colleagues (Fujita et al, 1989;Sano et al, 1993) described two monoclonal antibodies to glycosaminoglycan epitopes that recognize CSPGs that co-migrate on Western blots but that associate with the surfaces of different sets of neurons. Bertolotto et al (1990Bertolotto et al ( , 1991Bertolotto et al ( , 1996 described the distribution of CSPGs in adult brain using monoclonal antibodies that recognize the unsulfated, 4-sulfated, or 6-sulfated disaccharides that are exposed on CSPGs after chondroitinase digestion (Caterson et al, 1985). Each of these antibodies also recognizes a distinct set of neurons, which in cat visual cortex is different from the sets recognized by Cat-301 , .…”

Section: Discussionmentioning

confidence: 99%

A Family of Activity-Dependent Neuronal Cell-Surface Chondroitin Sulfate Proteoglycans in Cat Visual Cortex

et al. 1997

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Monoclonal antibody Cat-301 recognizes a chondroitin sulfate proteoglycan (CSPG) expressed on the extracellular surface of cell bodies and proximal dendrites of specific subsets of neurons in many areas of the mammalian CNS, including the cat visual cortex. The Cat-301 CSPG is first detected at the close of the critical period in development, a period during which the pattern of neuronal activity determines the mature synaptic circuitry and neuronal phenotype. In the cat visual cortex, dark-rearing from birth prolongs the duration of the critical period and attenuates the expression of the Cat-301 antigen, implicating the Cat-301 CSPG in the cellular mechanisms that terminate the period of synaptic plasticity. Because the Cat-301 antigen is expressed on only a limited subset of neurons, we have further examined the molecular heterogeneity among neuronal cell-surface CSPGs and have asked (1) whether other neuronal subsets carry distinct CSPGs and (2) whether the activity-dependent expression of the Cat-301 CSPG is a property generalizable to related cell-surface CSPGs. Here, we report two new monoclonal antibodies, Cat-315 and Cat-316, which together with Cat-301 define a family of at least seven related yet distinct CSPGs. These three antibodies define nonidentical subsets of neurons in the cat visual cortex. The expression of normal levels of these CSPGs is reduced by darkrearing. Together, these data show that the family of cellsurface CSPGs is molecularly diverse, that different sets of neurons express distinct complements of cell-surface antigens, and that the regulation of CSPG expression by activity may be a general feature of neuronal cell-surface CSPGs.

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“…The major extracellular matrix constituents of PNs have been characterized as chondroitin sulphate proteoglycans (CSPGs) that are members of the aggrecanversican-neurocan-brevican family of aggregating proteoglycans (Zaremba et al, 1989;Brü ckner et al, 1994Brü ckner et al, , 1998Asher et al, 1995;Bertolotto et al, 1996;Lander et al, 1997;Matsui et al, 1998Matsui et al, , 1999Hagihara et al, 1999;Yamaguchi, 2000). These proteoglycans usually occur complexed with hyaluronan (Delpech et al, 1982(Delpech et al, , 1989Brü ckner et al, 1993;Yasuhara et al, 1994;Köppe et al, 1997b).…”

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confidence: 93%

Postnatal development of perineuronal nets in wild-type mice and in a mutant deficient in tenascin-R

et al. 2000

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The extracellular matrix glycoprotein tenascin-R (TN-R), colocalizing with hyaluronan, phosphacan, and aggregating chondroitin sulphate proteoglycans in the white and grey matter, is accumulated in perineuronal nets that surround different types of neurons in many brain regions. To characterize the role of TN-R in the formation of perineuronal nets, we studied their postnatal development in wild-type mice and in a TN-R knock-out mutant by using the lectin Wisteria floribunda agglutinin and an antibody to nonspecified chondroitin sulphate proteoglycans as established cytochemical markers. We detected the matrix components TN-R, hyaluronan, phosphacan, neurocan, and brevican in the perineuronal nets of cortical and subcortical regions. In wild-type mice, lectin-stained, immature perineuronal nets were first seen on postnatal day 4 in the brainstem and on day 14 in the cerebral cortex. The staining intensity of these nets for TN-R, hyaluronan, phosphacan, neurocan, and brevican was extremely weak or not distinguishable from that of the surrounding neuropil. However, all markers showed an increase in staining intensity of perineuronal nets reaching maximal levels between postnatal days 21 and 40. In TN-R-deficient animals, the perineuronal nets tended to show a granular component within their lattice-like structure at early stages of development. Additionally, the staining intensity in perineuronal nets was reduced for brevican, extremely low for hyaluronan and neurocan, and virtually no immunoreactivity was detectable for phosphacan. The granular configuration of perineuronal nets became more predominant with advancing age of the mutant animals, indicating the continued abnormal aggregation of chondroitin sulphate proteoglycans complexed with hyaluronan. As shown by electron microscopy in the cerebral cortex, the disruption of perineuronal nets was not accompanied by apparent changes in the synaptic structure on net-bearing neurons. The regional distribution patterns and the temporal course of development of perineuronal nets were not obviously changed in the mutant. We conclude that the lack of TN-R initially and continuously disturbs the molecular scaffolding of extracellular matrix components in perineuronal nets. This may interfere with the development of the specific micromilieu of the ensheathed neurons and adjacent glial cells and may also permanently change their functional properties.

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Immunohistochemical mapping of perineuronal nets containing chondroitin unsulfate proteoglycan in the rat central nervous system

Cited by 70 publications

References 44 publications

Combining an Autologous Peripheral Nervous System “Bridge” and Matrix Modification by Chondroitinase Allows Robust, Functional Regeneration beyond a Hemisection Lesion of the Adult Rat Spinal Cord

Combining an Autologous Peripheral Nervous System “Bridge” and Matrix Modification by Chondroitinase Allows Robust, Functional Regeneration beyond a Hemisection Lesion of the Adult Rat Spinal Cord

A Family of Activity-Dependent Neuronal Cell-Surface Chondroitin Sulfate Proteoglycans in Cat Visual Cortex

Postnatal development of perineuronal nets in wild-type mice and in a mutant deficient in tenascin-R

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