Perineuronal Nets of Proteoglycans in the Adult Mouse Brain, with Special Reference to Their Reactions to Goemoeri's Ammoniacal Silver and Ehrlich's Methylene Blue.

Murakami, Takuro; Murakami, Tetsuro; Sato, Hiroyuki; Mubarak, W.; Ohtsuka, Aiji; Abe, Kōji

doi:10.1679/aohc.62.71

Cited by 13 publications

(5 citation statements)

References 51 publications

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“…CSPGs are major components of the brain ECM. Thought to be the ‘organizers’ of the ECM (Yamaguchi, 2000), CSPGs are key functional elements of PNNs, perinodal ECM and CS6 clusters (Bandtlow & Zimmermann, 2000; Bekku & Oohashi, 2010; Bekku et al., 2009; Carulli et al., 2005, 2006; Chelini et al., 2018; Dours‐Zimmermann et al., 2009; Fawcett et al., 2019; Hartig et al., 1994; Hayashi et al., 2007; Horii‐Hayashi et al., 2008, 2010; Hunanyan et al., 2010; Kwok et al., 2011; Maeda et al., 2010; Matthews et al., 2002; Matuszko et al., 2017; Melendez‐Vasquez et al., 2005; Murakami et al., 1999; Murakami & Ohtsuka, 2003; Pantazopoulos et al., 2015; Petrosyan et al., 2013; Seidenbecher et al., 2002; Vitellaro‐Zuccarello et al., 2001). Among the brain CSPGs, ACAN, BCAN, VCAN and NCAN prominently contribute to the composition of PNNs, regulating their functions (Deepa et al., 2006; Giamanco & Matthews, 2012; Giamanco et al., 2010; Suttkus et al., 2014).…”

Section: Discussionmentioning

confidence: 99%

Molecular signature of extracellular matrix pathology in schizophrenia

Pantazopoulos

Katsel

Haroutunian

et al. 2020

Eur J of Neuroscience

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Growing evidence points to a critical involvement of the extracellular matrix (ECM) in the pathophysiology of schizophrenia (SZ). Decreases of perineuronal nets (PNNs) and altered expression of chondroitin sulphate proteoglycans (CSPGs) in glial cells have been identified in several brain regions. GWAS data have identified several SZ vulnerability variants of genes encoding for ECM molecules. Given the potential relevance of ECM functions to the pathophysiology of this disorder, it is necessary to understand the extent of ECM changes across brain regions, their region-and sexspecificity and which ECM components contribute to these changes. We tested the hypothesis that the expression of genes encoding for ECM molecules may be broadly disrupted in SZ across several cortical and subcortical brain regions and include key ECM components as well as factors such as ECM posttranslational modifications and regulator factors. Gene expression profiling of 14 neocortical brain regions, caudate, putamen and hippocampus from control subjects (n = 14/region) and subjects with SZ (n = 16/region) was conducted using Affymetrix microarray analysis. Analysis across brain regions revealed widespread dysregulation of ECM gene expression in cortical and subcortical brain regions in SZ, impacting several ECM functional key components. SRGN, CD44, ADAMTS1, ADAM10, BCAN, NCAN and SEMA4G showed some of the most robust changes. Region-, sex-and age-specific gene expression patterns and correlation with cognitive scores were also detected. Taken together, these findings contribute to emerging evidence for large-scale ECM dysregulation in SZ and point to molecular pathways involved in PNN decreases, glial cell dysfunction and cognitive impairment in SZ.This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Section: Discussionmentioning

confidence: 99%

Molecular signature of extracellular matrix pathology in schizophrenia

Pantazopoulos

Katsel

Haroutunian

et al. 2020

Eur J of Neuroscience

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“…There have been several mechanisms proposed for attaching PNNs to neurons including a collagenous ligand (Murakami et al ., 1999a; Murakami et al ., 1999b), cell surface‐associated CSPGs such as aggrecan (Koppe et al ., 1997; Lander et al ., 1997; Matthews et al ., 2002), brevican (Seidenbecher et al ., 2002) and transmembrane CSPGs such as NG2, neuroglycan C and phosphacan (Fox & Caterson, 2002). RPTPβ, as a transmembrane form of phosphacan, has recently been shown to be expressed by both neurons and glia; it could act as a link between PNNs and neurons (Margolis et al ., 1996; Margolis & Margolis, 1997; Hayashi et al ., 2005; Heck et al ., 2005).…”

Section: Discussionmentioning

confidence: 99%

Distribution and synthesis of extracellular matrix proteoglycans, hyaluronan, link proteins and tenascin‐R in the rat spinal cord

Galtrey¹,

Kwok²,

Carulli

et al. 2008

Eur J of Neuroscience

175

182

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Perineuronal nets (PNNs) are dense extracellular matrix (ECM) structures that form around many neuronal cell bodies and dendrites late in development. They contain several chondroitin sulphate proteoglycans (CSPGs), hyaluronan, link proteins and tenascin-R. Their time of appearance correlates with the ending of the critical period for plasticity, and they have been implicated in this process. The distribution of PNNs in the spinal cord was examined using Wisteria floribunda agglutinin lectin and staining for chondroitin sulphate stubs after chondroitinase digestion. Double labelling with the neuronal marker, NeuN, showed that PNNs were present surrounding approximately 30% of motoneurons in the ventral horn, 50% of large interneurons in the intermediate grey and 20% of neurons in the dorsal horn. These PNNs formed in the second week of postnatal development. Immunohistochemical staining demonstrated that the PNNs contain a mixture of CSPGs, hyaluronan, link proteins and tenascin-R. Of the CSPGs, aggrecan was present in all PNNs while neurocan, versican and phosphacan/RPTPbeta were present in some but not all PNNs. In situ hybridization showed that aggrecan and cartilage link protein (CRTL 1) and brain link protein-2 (BRAL 2) are produced by neurons. PNN-bearing neurons express hyaluronan synthase, and this enzyme and phosphacan/RPTPbeta may attach PNNs to the cell surface. During postnatal development the expression of link protein and aggrecan mRNA is up-regulated at the time of PNN formation, and these molecules may therefore trigger their formation.

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“…Specific activity was detected using an ABC reagent (1:100; Vector Laboratories Inc, Burlington CA) and visualized with 3, 3-diaminobenzidine (0.5 mg/ml) and hydrogen peroxide (0.03%) in buffer solution (DAB peroxidase kit; Vector Laboratories). To determine chondroitin sulfate proteoglycan (CSPG) composition, sections were processed for wisteria floribunda agglutinin (WFA) which recognizes N-acetylgalactosamine, a sugar that is found in the glycosaminoglycan chains of CSPGs (Murakami et al, 1999 ). Sections (C57Bl/6: ND = 5, 2dMD = 4, 4dMD = 4, 7dMD = 4; MMP9 KO ND = 5, 2dMD = 5, 4dMD = 5, 7dMD = 5) were processed free-floating by first blocking sequentially in a streptavidin and biotin solution (Biotin/Streptavidin Block Kit, Vector Labs, SP-2002, per kit instructions).…”

Section: Methodsmentioning

confidence: 99%

Proteolytic regulation of synaptic plasticity in the mouse primary visual cortex: analysis of matrix metalloproteinase 9 deficient mice

Russo

Jackson

Lamantia

et al. 2015

Front. Cell. Neurosci.

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The extracellular matrix (ECM) is known to play important roles in regulating neuronal recovery from injury. The ECM can also impact physiological synaptic plasticity, although this process is less well understood. To understand the impact of the ECM on synaptic function and remodeling in vivo, we examined ECM composition and proteolysis in a well-established model of experience-dependent plasticity in the visual cortex. We describe a rapid change in ECM protein composition during Ocular Dominance Plasticity (ODP) in adolescent mice, and a loss of ECM remodeling in mice that lack the extracellular protease, matrix metalloproteinase-9 (MMP9). Loss of MMP9 also attenuated functional ODP following monocular deprivation (MD) and reduced excitatory synapse density and spine density in sensory cortex. While we observed no change in the morphology of existing dendritic spines, spine dynamics were altered, and MMP9 knock-out (KO) mice showed increased turnover of dendritic spines over a period of 2 days. We also analyzed the effects of MMP9 loss on microglia, as these cells are involved in extracellular remodeling and have been recently shown to be important for synaptic plasticity. MMP9 KO mice exhibited very limited changes in microglial morphology. Ultrastructural analysis, however, showed that the extracellular space surrounding microglia was increased, with concomitant increases in microglial inclusions, suggesting possible changes in microglial function in the absence of MMP9. Taken together, our results show that MMP9 contributes to ECM degradation, synaptic dynamics and sensory-evoked plasticity in the mouse visual cortex.

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Perineuronal Nets of Proteoglycans in the Adult Mouse Brain, with Special Reference to Their Reactions to Goemoeri's Ammoniacal Silver and Ehrlich's Methylene Blue.

Cited by 13 publications

References 51 publications

Molecular signature of extracellular matrix pathology in schizophrenia

Molecular signature of extracellular matrix pathology in schizophrenia

Distribution and synthesis of extracellular matrix proteoglycans, hyaluronan, link proteins and tenascin‐R in the rat spinal cord

Proteolytic regulation of synaptic plasticity in the mouse primary visual cortex: analysis of matrix metalloproteinase 9 deficient mice

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