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Aged somatosensory cortex displays increased densities of perineuronal nets that are not associated with GAD-positive neurons

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Nowicka D., Karetko-Sysa M., Skangiel-Kramska J.

Acta Neurobiologiae Experimentalis

2011

tom 71

nr S

Ageing of the brain results in some degree of decline in a number of functions, one of which is neuronal plasticity. Recently, perineuronal nets (PNNs), a structuralized form of the brain extracellular matrix observed around some neurons (often GABAergic) have been postulated as a molecular brake, actively preventing plasticity in the adult brain. Removal of PNNs in visual cortex results in the restoration of ocular dominance plasticity in adult mice, and knockout mice with attenuated PNNs retain juvenile levels of ocular dominance plasticity. Little data, however, exist on the expression and function of PNNs in aged animals. We examined whether the decrease in neuronal plasticity during ageing could be the result of gradual increase in PNN density. To this aim we investigated PNNs across the layers of the somatosensory cortex of the adult (3 months) and aged (1 year) mouse. To visualize PNNs we employed Wisteria floribunda (WFA) lectin, binding to the sugar epitopes of PNNs, and CAT315 antibody recognizing a specific glycoform of PNN constituent, aggrecan. GAD and parvalbumin (PV) antibodies were used to stain GABAergic neurons. Detailed microscopic analysis revealed that in aged animals the density of WFA-positive PNNs increased significantly in layers IV and V-VI. At the same time the density of CAT-315-positive PNNs decreased slightly, thus suggesting changes in PNN composition. Co-localization studies revealed that the observed increase was mostly confined to WFA+/CAT-315 neurons that did not contain PV. Moreover, this increase in enveloping was characteristic for neurons that were GAD-negative. Ageing had no influence on the density of GADpositive or PV-positive cells. Our results suggest that in aged animals some additional set of neurons was enveloped by PNNs, possibly contributing to further limiting of cortical plasticity. Interestingly, these neurons are not necessarily GABAergic.

Aging does not alter the distribution and the densities of parvalbumin-, calretinin and calbindin-positive neurons in the mouse somatosensory cortex

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Nowicka D., Karetko-Sysa M., Skangiel-Kramska J.

Acta Neurobiologiae Experimentalis

2013

tom 73

nr Suppl.1

Gabaergic interneurons are involved in regulating developmental plasticity of visual, auditory and somatosensory cortices, as well as in learning and memory processes. It has been suggested that age related worsening of brain function and plasticity could be, at least in part, attributed to alterations in gabaergic system. Gabaergic interneurons constitute a heterogeneous cell population classified into groups based on their calcium binding protein content. In the present study, we evaluate with immunohistochemistry technique the effect that aging has on the three of them, namely Parvalbumin (PV)-, Calbindin (CB)- and Calretinin (CR)-expressing neurons, in the somatosensory cortex of young (3 month old) and middleaged (1 year old) mice. We found that the distribution across layers differs between neuron types. PV-positive neurons were observed across the thickness of the cortex, with highest densities in layer IV. CB-positive neurons were much less numerous than the latter, and were observed in layers II/III and V/VI. Layer IV was practically devoid of CB-positive neurons. CR-positive neurons were scarcely distributed across all layers, with lower densities in layers V/VI. We did not observe the effect of age in neither of the neuron type examined. It suggested that age-dependent decline of somatosensory cortex plasticity does not depend on gabaergic neuron loss.

Ograniczanie wyników

2 Acta Neurobiologiae Experimentalis

2 Karetko-Sysa M.

2 Nowicka D.

2 Skangiel-Kramska J.

1 2013

1 2011

Wyniki wyszukiwania

Aged somatosensory cortex displays increased densities of perineuronal nets that are not associated with GAD-positive neurons

Aging does not alter the distribution and the densities of parvalbumin-, calretinin and calbindin-positive neurons in the mouse somatosensory cortex