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Related Concept Videos

Neurogenesis and Regeneration of Nervous Tissue01:15

Neurogenesis and Regeneration of Nervous Tissue

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In the CNS, neurogenesis, the birth of new neurons from stem cells, is limited to the hippocampus in adults. In other regions of the brain and spinal cord, neurogenesis is almost non-existent due to inhibitory influences from neuroglia, especially oligodendrocytes, and the absence of growth-stimulating cues. The myelin produced by oligodendrocytes in the CNS inhibits neuronal regeneration. Furthermore, astrocytes proliferate rapidly after neuronal damage, forming scar tissue that physically...
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Related Experiment Video

Updated: Jun 21, 2025

Experimental Demyelination and Remyelination of Murine Spinal Cord by Focal Injection of Lysolecithin
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GCPII Inhibition Promotes Remyelination after Peripheral Nerve Injury in Aged Mice.

Yu Su1,2, Meixiang Huang1,2, Ajit G Thomas1

  • 1Johns Hopkins Drug Discovery, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

International Journal of Molecular Sciences
|July 13, 2024
PubMed
Summary
This summary is machine-generated.

Inhibiting glutamate carboxypeptidase II (GCPII) with 2-PMPA enhanced nerve repair in aged mice. This therapy shows promise for improving remyelination and recovery from peripheral nerve injuries, especially in older adults.

Keywords:
GCPIIPNISchwann cellsagingmacrophagesremyelination

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Area of Science:

  • Neuroscience
  • Regenerative Medicine
  • Pharmacology

Background:

  • Peripheral nerve injuries (PNIs) present significant challenges, particularly in the elderly, due to impaired regeneration.
  • Glutamate carboxypeptidase II (GCPII) regulates glutamate signaling and is upregulated in aging and following PNIs.
  • GCPII is found in Schwann cells and macrophages within the peripheral nervous system (PNS).

Purpose of the Study:

  • To investigate the therapeutic potential of inhibiting GCPII activity for enhancing PNI repair.
  • To evaluate the effects of the GCPII inhibitor 2-PMPA on remyelination and nerve regeneration.

Main Methods:

  • Assessed GCPII expression and activity post-PNI in aged mice.
  • Administered 2-PMPA, a selective GCPII inhibitor, in vitro and in vivo.
  • Utilized dorsal root ganglion (DRG) explants for in vitro myelination studies.
  • Employed a sciatic nerve crush injury model in aged mice for in vivo assessment.

Main Results:

  • PNI significantly increased GCPII protein and activity, which was normalized by 2-PMPA.
  • In vitro, 2-PMPA treatment robustly enhanced myelination in DRG explants.
  • In vivo, 2-PMPA accelerated remyelination in aged mice, increasing myelin sheath thickness and the number of remyelinated axons.

Conclusions:

  • GCPII inhibition represents a potential therapeutic strategy to improve remyelination after PNI.
  • This approach is particularly relevant for elderly patients, where natural repair mechanisms are compromised.
  • Further research may explore GCPII inhibition for enhancing functional recovery following peripheral nerve damage.