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Related Experiment Video

Updated: Jun 12, 2026

Assessment of Ultrastructural Neuroplasticity Parameters After In Utero Transduction of the Developing Mouse Brain and Spinal Cord

Assessment of Ultrastructural Neuroplasticity Parameters After In Utero Transduction of the Developing Mouse Brain and Spinal Cord

Published on: February 26, 2019

Animals lacking link protein have attenuated perineuronal nets and persistent plasticity.

Daniela Carulli¹, Tommaso Pizzorusso, Jessica C F Kwok

¹Cambridge University Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Robinson Way, Cambridge, CB2 0PY, UK.

Brain : a Journal of Neurology

|June 23, 2010

Summary

Cartilage link protein Crtl1 (Hapln1) forms chondroitin sulphate proteoglycan nets, restricting central nervous system plasticity. Removing Crtl1 preserves plasticity and visual acuity, identifying net formation as key to plasticity control.

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Last Updated: Jun 12, 2026

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Area of Science:

Neuroscience
Developmental Biology
Extracellular Matrix Biology

Background:

Chondroitin sulphate proteoglycans (CSPGs) in the extracellular matrix inhibit central nervous system (CNS) plasticity.
The specific ECM structures responsible for this plasticity restriction remain unidentified.
Changes in CSPG levels, glycosaminoglycan sulphation, and perineuronal net (PNN) formation occur as critical periods for plasticity close.

Purpose of the Study:

To identify the specific extracellular matrix structures that restrict CNS plasticity.
To investigate the role of cartilage link protein Crtl1 (Hapln1) in PNN formation and CNS plasticity.

Main Methods:

Utilized Crtl1 knockout mice to assess PNN formation and plasticity.
Analyzed changes in CSPGs, glycosaminoglycan sulphation, and PNNs in wild-type and knockout animals.
Examined ocular dominance plasticity and visual acuity after visual deprivation in Crtl1 knockout mice.
Investigated axonal sprouting in the sensory pathway of knockout and control animals.

Main Results:

Neuronal production of Crtl1 triggers PNN formation.
Mice lacking Crtl1 exhibited attenuated PNNs, but CSPG levels and sulphation patterns were unaltered.
Crtl1 knockout animals maintained juvenile levels of ocular dominance plasticity and sensitivity to visual deprivation.
Axons in Crtl1 knockout animals showed sprouting into denervated areas, unlike controls.

Conclusions:

The organization of CSPGs into PNNs, mediated by Crtl1, is the critical factor controlling CNS plasticity.
Crtl1 plays a crucial role in regulating the timing and extent of plasticity closure in the CNS.
Targeting PNN formation offers a potential strategy for reactivating plasticity in the adult CNS.