A comparison between Perineuronal Nets and Parvalbumin neurons expression in Retrosplenial cortex in two different models: model of aging and model of Fragile X Syndrome disease.

This study investigates the expression of parvalbumin (PV) and perineuronal net (PNN) positive (+) neurons in the retrosplenial cortex (RSC) of a mouse model of aging and in the Fmr1 knockout (KO), a model of the Fragile X Syndrome (FXS). The RSC is crucial for cognitive functions and is notably susceptible to changes associated with different environmental conditions. PV+ neurons, which are a subset of GABAergic interneurons, play a vital role in maintaining cortical excitability and synchrony, while PNNs are specialized extracellular matrix (ECM) structures that enwrap certain neurons, including PV+ neurons, and regulate their function and plasticity. PNN development and maintenance is necessary for regulation of GABAergic cell function and are important brakes of plasticity. Many evidences have documented alteration of PV+ neuron and PNN expression in several neurological disorders. In aging, data are showing changes in PNN expression patterns and molecular composition and in PV+ neuron density in the entire cortex; alterations that reflect decreased neuronal plasticity and increased vulnerability to cognitive decline. On the other hand, in some brain areas of FXS models, as well as in affected humans, it has been documented an impairment of PNN development, and consequently of PV+ cell maturation. However, all these alterations are species- and region-specific, and little is known about the RSC. Here we try to highlight the differential impacts of aging and FXS on RSC plasticity, and to do so we employed immunohistochemistry to quantify and compare the density and distribution of PNN+ and PV+ neurons in this area.