Abstract
Brain cells are immersed in a complex structure forming the extracellular matrix. The composition of the matrix gradually matures during postnatal development, as the brain circuitry reaches its adult form. The fully developed extracellular environment stabilizes neuronal connectivity and decreases cortical plasticity as highlighted by the demonstration that treatments degrading the matrix are able to restore synaptic plasticity in the adult brain. The mechanisms through which the matrix inhibits cortical plasticity are not fully clarified. Here we show that a prominent component of the matrix, chondroitin sulfate proteoglycans (CSPGs), restrains morphological changes of dendritic spines in the visual cortex of adult mice. By means of in vivo and in vitro two-photon imaging and electrophysiology, we find that after enzymatic digestion of CSPGs, cortical spines become more motile and express a larger degree of structural and functional plasticity.
Highlights
Brain cells are immersed in a complex structure forming the extracellular matrix
The occipital cortex of mice expressing green fluorescent protein (GFP) in a sparse set of layer 5 (L5) pyramidal neurons[26] (Thy1-GFP mice) was injected with either chondroitinase ABC (ChABC) or penicillinase; we show that 3 days later chondroitin sulfate proteoglycans (CSPGs) were strongly degraded in the ChABC-injected cortex, whereas the control treatment had no effects and the integrity of the perineuronal nets and of the diffuse staining for CSPGs was preserved (Fig. 1a)
Our data suggest that the increased spine plasticity caused by the degradation of CSPGs leads to an increased susceptibility to activity-dependent potentiation of excitatory connectivity
Summary
Brain cells are immersed in a complex structure forming the extracellular matrix. The composition of the matrix gradually matures during postnatal development, as the brain circuitry reaches its adult form. In spite of the accumulating evidence for the role of CSPGs as stabilizers of synaptic connectivity, little is known about the mechanisms underlying the plasticity reinstatement that follows CSPGs degradation The search for this can be inspired by the inhibitory effects of CSPGs on axonal sprouting that suggest a direct restraining action on the structural remodeling of neurons. Removal of CSPGs followed by high frequency activity allows the potentiation of visual responses together with the enlargement of spine heads These data show that the degradation of CSPGs in the adult visual cortex allows the potentiation of existing synapses at a very short time scale and the formation of new synaptic contacts at a longer time scale
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