Synaptic circuit remodelling by matrix metalloproteinases in health and disease

Huntley, George W.

doi:10.1038/nrn3320

Cited by 246 publications

(300 citation statements)

References 155 publications

(212 reference statements)

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“…It is also known that experience modifies functional circuits in the brain (2) and that changes in the morphology of dendritic spines might be involved in synaptic plasticity related to learning and memory (3,4). Notably, synaptic plasticity involves remodeling of the extracellular matrix in the brain (5)(6)(7)(8).…”

mentioning

confidence: 99%

Matrix Metalloproteinase (MMP) 9 Transcription in Mouse Brain Induced by Fear Learning

Ganguly¹,

Rejmak²,

Mikosz

et al. 2013

Journal of Biological Chemistry

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Background: Matrix metalloproteinase 9 is involved in fear-associated memory formation wherein transcriptional regulation is poorly known. Results: Overexpression and promoter binding activity of AP-1 factors regulate MMP-9 transcription, preceding elevated enzymatic activity in mouse brain. Conclusion: c-Fos and c-Jun AP-1 components positively regulate MMP-9 transcription in fear learning. Significance: The novel tools and approaches in vivo allowed us to explore MMP-9 transcription in mouse brain.

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mentioning

confidence: 99%

Matrix Metalloproteinase (MMP) 9 Transcription in Mouse Brain Induced by Fear Learning

Ganguly¹,

Rejmak²,

Mikosz

et al. 2013

Journal of Biological Chemistry

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“…MMP activity can switch from harmful to reparative, allowing axon re-growth, remyelination and re-establishment of connectivity (Yong 2005;Agrawal et al 2008, Huntley 2012De Stefano et al 2012). In particular, oligodendrocyte-derived MMP-9 supports oligodendrogliosis and myelin restoration (Uhm et al 1998;Oh et al 1999;Larsen et al 2003).…”

Section: Discussionmentioning

confidence: 99%

Metalloproteinase-9 contributes to inflammatory glia activation and nigro-striatal pathway degeneration in both mouse and monkey models of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinsonism

et al. 2014

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Inflammation is a predominant aspect of neurodegenerative diseases, manifested by glia activation and expression of pro-inflammatory mediators. Studies on animal models of Parkinson's disease (PD) suggest that sustained neuroinflammation exacerbates degeneration of the dopaminergic (DA) nigro-striatal pathway. Therefore, insights into the inflammatory mechanisms of PD may help the development of novel therapeutic strategies against this disease. As extracellular matrix metalloproteinases (MMPs) could be major players in the progression of Parkinsonism, we investigated, in the substantia nigra and striatum of mice acutely injected with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), changes in mRNA expression, protein levels, and cell localization of MMP-9. This protease is mainly neuronal, but early after MPTP injection its mRNA and protein levels, as well as the number of MMP-9-expressing microglia and astrocytes, increase concomitantly to a prominent inflammation. Neuroinflammation and MMP-9+ glia begin to decline within 2 weeks, although protein levels remain higher than control, in association with a partial recovery of DA nigro-striatal circuit. Comparable quantitative studies on MMP-9 knock-out mice, show a significant decrease in both glia activation and loss of DA neurons and fibers, with respect to wild-type. Moreover, in a parallel study on chronically MPTP-injected macaques, we observed that perpetuation of inflammation and high levels of MMP-9 are associated to DA neuron loss. Our data suggest that MMP-9 released by injured neurons favors glia activation; glial cells in turn reinforce their reactive state via autocrine MMP-9 release, contributing to nigro-striatal pathway degeneration. Specific modulation of MMP-9 activity may, therefore, be a strategy to ameliorate harmful inflammatory outcomes in Parkinsonism. © 2014 Springer-Verlag Berlin Heidelberg

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“…Unparalleled quality and customer service has made us the leading distributor of fine European surgical instruments worldwide. [ 7 ]. Dadurch werden temporär lokale Bereiche "juveniler" plastischer Formbarkeit erzeugt, was die Balance zwischen Flexibilität und Stabilität im reifen Gehirn maßgeblich bestimmt.…”

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Einfluss der Extrazellulären Matrix auf plastische Prozesse in jungen und alten Gehirnen. Extrazelluläre Matrix und Hirnplastizität

Frischknecht¹,

Happel²

2016

E-Neuroforum

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ZusammenfassungDie Balance zwischen struktureller Stabilität und funktioneller Flexibilität synaptischer Schaltkreise passt sich im Gehirn höherer Vertebraten ständig an die verschiedenen Lebensumstände an. Zunächst herrscht im juvenilen Hirnstadium hohe strukturelle Plastizität. Als kritischer Schritt in der Hirnreifung gilt die Entstehung der Extrazellulären Matrix (ECM, aus dem Englischen extracellular matrix ), welche das Potenzial für neuronale Plastizität und Regeneration als strukturstabilisierende Einheit limitiert. Neueste Forschungen haben erst begonnen, den Einfluss dieser vermeintlichen Limitierung adulter Plastizität auf lernabhängige Plastizität, lebenslange Gedächtnisanpassungen und höhere kognitive Funktionen zu untersuchen. In diesem Übersichtsartikel fassen wir aktuelle Befunde zusammen, welche die aktivitätsabhängige Modulation der ECM als Schlüsselelement für die Regulation lernabhängiger Plastizität im adulten Gehirn beschreiben. Die experimentelle Modifikation der ECM in lokalen neuronalen Schaltkreisen kann darüber hinaus als Werkzeug genutzt werden, um kurze Zeitfenster aktivitätsabhängiger neuronaler Reorganisationen zu ermöglichen. Wir diskutieren die Einflüsse dieser Verfahren auf entwicklungsabhängige Plastizität sowie Möglichkeiten der kognitiv flexibleren Auswahl wahrend unterschiedlicher Lern- und Verhaltensoptionen. Diese Befunde bieten Implikationen für neue regenerative und therapeutische Konzepte basierend auf zielgerichteter Neuroplastizität.

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Synaptic circuit remodelling by matrix metalloproteinases in health and disease

Cited by 246 publications

References 155 publications

Matrix Metalloproteinase (MMP) 9 Transcription in Mouse Brain Induced by Fear Learning

Matrix Metalloproteinase (MMP) 9 Transcription in Mouse Brain Induced by Fear Learning

Metalloproteinase-9 contributes to inflammatory glia activation and nigro-striatal pathway degeneration in both mouse and monkey models of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinsonism

Einfluss der Extrazellulären Matrix auf plastische Prozesse in jungen und alten Gehirnen. Extrazelluläre Matrix und Hirnplastizität

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