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Extracellular Matrix Modulation Is Driven by Experience-Dependent Plasticity During Stroke Recovery.

Miriana Jlenia Quattromani1, Mathilde Pruvost2, Carla Guerreiro3

  • 1Laboratory for Experimental Brain Research, Division of Neurosurgery, Department of Clinical Sciences, Lund University, BMC A13, 22184, Lund, Sweden. miriana.quattromani@med.lu.se.

Molecular Neurobiology
|March 15, 2017
PubMed
Summary
This summary is machine-generated.

An enriched environment (EE) after stroke improves motor function by reducing perineuronal nets (PNNs) and modulating extracellular matrix (ECM) proteases, offering potential therapeutic targets for stroke recovery.

Keywords:
Experience-dependent plasticityExtracellular matrixPerineuronal netsProteasesSomatosensory cortexStroke recovery

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Area of Science:

  • Neuroscience
  • Neuroplasticity
  • Extracellular Matrix Biology

Background:

  • Stroke induces brain injury and subsequent tissue remodeling.
  • Experience-dependent brain plasticity, facilitated by enriched environments (EE), promotes recovery after central nervous system injury.
  • Perineuroneal nets (PNNs), composed of chondroitin sulfate proteoglycans, inhibit neural plasticity and are found around specific neurons (PV/GABA).

Purpose of the Study:

  • To investigate the role of extracellular matrix (ECM) proteases and their inhibitors in regulating PNN integrity during stroke recovery.
  • To determine the effects of an enriched environment (EE) on PNNs and associated proteolytic activity post-stroke.
  • To identify potential molecular targets for enhancing stroke rehabilitation therapies.

Main Methods:

  • Photothrombotic stroke model in rats, followed by assessment of functional deficits.
  • Housing rats in standard or enriched environments (EE) to evaluate behavioral recovery and infarct size.
  • Immunohistochemical analysis of PNNs, RT-qPCR for ECM protease/inhibitor mRNA, and gel zymography for protease activity.
  • Analysis of PNNs and protease activity in human stroke patient brains.

Main Results:

  • EE administration post-stroke significantly improved behavioral recovery of limb-placement ability without altering infarct volume.
  • EE led to a reduction in PNNs surrounding parvalbumin-containing GABAergic (PV/GABA) neurons in the somatosensory cortex.
  • EE modulated the expression and activity of ECM proteases and protease inhibitors in the affected brain region.
  • Similar changes in PNNs and protease activity were observed in human stroke patient brains.

Conclusions:

  • Enriched environments promote functional recovery after stroke by remodeling the extracellular matrix, specifically by reducing PNNs.
  • Modulation of ECM proteases and their inhibitors represents a promising therapeutic strategy to enhance neuroplasticity and support stroke rehabilitation.
  • This research identifies key molecular targets for developing novel interventions to aid stroke patient recovery.