Postnatal development of perineuronal nets in wild-type mice and in a mutant deficient in tenascin-R.

摘要: The extracellular matrix glycoprotein tenascin-R (TN-R), colocalizing with hyaluronan, phosphacan, and aggregating chondroitin sulphate proteoglycans in the white grey matter, is accumulated perineuronal nets that surround different types of neurons many brain regions. To characterize role TN-R formation nets, we studied their postnatal development wild-type mice a knock-out mutant by using lectin Wisteria floribunda agglutinin an antibody to nonspecified as established cytochemical markers. We detected components TN-R, neurocan, brevican cortical subcortical In mice, lectin-stained, immature were first seen on day 4 brainstem 14 cerebral cortex. staining intensity these for was extremely weak or not distinguishable from surrounding neuropil. However, all markers showed increase reaching maximal levels between days 21 40. TN-R-deficient animals, tended show granular component within lattice-like structure at early stages development. Additionally, reduced brevican, low hyaluronan virtually no immunoreactivity detectable phosphacan. configuration became more predominant advancing age indicating continued abnormal aggregation complexed hyaluronan. As shown electron microscopy cortex, disruption accompanied apparent changes synaptic net-bearing neurons. regional distribution patterns temporal course obviously changed mutant. conclude lack initially continuously disturbs molecular scaffolding nets. This may interfere specific micromilieu ensheathed adjacent glial cells also permanently change functional properties.