Role in Neuroplasticity
PNNs play an important role in neuroplasticity. Traumatic injury of the CNS results in degeneration of denervated and damaged neurons, the formation of a glial scar, and collateral sprouting of surviving neurons. PNNs have been shown to be inhibitory to axonal regeneration and outgrowth. CSPGs are the main axon growth inhibitory molecules in the glial scar that play a role in the failure of the axon to regenerate after injury. In the rat brain and spinal cord, the expression of various CSPGs (brevican, versican, neurocan, and NG2) increases after injury. In vivo treatment with ChABC results in the enhancement of the regeneration of axons (specifically dopaminergic neurons) and the promotion of axon regeneration and functional recovery following spinal cord injury.
CSPGs and PNNs are also implicated in the restricted plasticity present after CNS injury. In the rat cerebellum, application of ChABC promotes structural plasticity of Purkinje axons. Following spinal cord injury, rats treated with ChABC show structural and functional recovery in the form of increased regrowth of axons into the denervated territory and the recovery of motor and bladder function. Plasticity of intact areas in the brain stem and spinal cord also increases following spinal cord injury.
Read more about this topic: Perineuronal Net
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