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Daniela Tropea

Publications and source records attributed to Daniela Tropea.

4 recordsLinked to original sources

Gene expression changes and molecular pathways mediating activity-dependent plasticity in visual cortex.

Two key models for examining activity-dependent development of primary visual cortex (V1) involve either reduction of activity in both eyes via dark-rearing (DR) or imbalance of activity between the two eyes via monocular deprivation (MD). Combining DNA microarray analysis with computational approaches, RT-PCR, immunohistochemistry and physiological imaging, we find that DR leads to (i) upregulation of genes subserving synaptic transmission and electrical activity, consistent with a coordinated response of cortical neurons to reduction of visual drive, and (ii) downregulation of parvalbumin expression, implicating parvalbumin-expressing interneurons as underlying the delay in cortical maturation after DR. MD partially activates homeostatic mechanisms but differentially upregulates molecular pathways related to growth factors and neuronal degeneration, consistent with reorganization of connections after MD. Expression of a binding protein of insulin-like growth factor-1 (IGF1) is highly upregulated after MD, and exogenous application of IGF1 prevents the physiological effects of MD on ocular dominance plasticity examined in vivo.

Animals↗

Neuronal activity regulates the developmental expression and subcellular localization of cortical BDNF mRNA isoforms in vivo.

Activity-dependent changes in BDNF expression have been implicated in developmental plasticity. Although its expression is widespread in visual cortex, developmental regulation of its different transcripts by visual experience has not been investigated. Here, we investigated the cellular expression of different BDNF transcripts in rat visual cortex during postnatal development. We found that transcripts I and II are expressed only in adults but III and IV are expressed from early postnatal stage. Total BDNF mRNA is expressed throughout the age groups. Transcripts III and IV show a differential intracellular localization, while former was detected only in cell bodies, latter is present both in cell bodies and dendritic processes. Inhibition of visual activity decreases the levels of exons, with exon IV transcript almost disappearing from dendrites. In vitro experiments also confirmed the above results, indicating activity-dependent regulation of different BDNF promoters with specific temporal and cellular patterns of expression in developing visual cortex.

Animals↗

Synergistic effects of brain-derived neurotrophic factor and chondroitinase ABC on retinal fiber sprouting after denervation of the superior colliculus in adult rats.

Damage to the adult CNS often causes devastating and permanent deficits because of the limited capacity of the brain for anatomical reorganization. The finding that collateral sprouting of uninjured fiber tracts mediates recovery of function prompts the search for experimental strategies that stimulate axonal plasticity after CNS trauma. Here we characterize treatments that promote the sprouting of undamaged retinal afferents into the denervated superior colliculus (SC) after a partial retinal lesion in the adult rat. Delivery of brain-derived neurotrophic factor (BDNF) was performed to enhance the intrinsic potential of retinal ganglion cells to reelongate their axons. Reduction of the neurite growth-inhibitory properties of the adult SC was accomplished via treatment with chondroitinase ABC (C-ABC), which degrades chondroitin sulfate proteoglycans. Retinal axons were labeled via intraocular injections of fluorescently tagged cholera toxin B subunit, and fiber sprouting within the denervated SC was measured by quantitative laser-scanning confocal microscopy 1 week after the retinal lesion. We found that both the administration of BDNF and the injection of C-ABC induce significant sprouting of retinal afferents into the collicular scotoma. Remarkably, the combined treatment with BDNF and C-ABC showed synergistic effects on axon growth. Colocalization analysis with anti-synapsin antibodies demonstrated synapse formation by the sprouting axons. These results suggest that the combined treatment with BDNF and C-ABC can be relevant in therapies for the repair of the damaged adult CNS.

Animals↗

Rat visual cortical neurones express TrkA NGF receptor.

In this study we report the expression of TrkA receptor within the rat visual cortex during postnatal development and in adulthood, using a specific monoclonal antibody which recognizes the extracellular domain of TrkA receptor. TrkA was not detected by immunohistochemistry at postnatal day 13 (P13), i.e. before eye opening. At P22 TrkA was mostly localised in cortical fibre-like processes. At P39 and P90, TrkA-positive neuronal cell bodies in supragranular and infragranular layers were found. Using double immunohistochemistry, labelled cells were identified as intrinsic cholinergic neurones, and as interneurones expressing calbindin and neuropeptide Y. We conclude that TrkA is expressed in visual cortical neurones during postnatal development and in adulthood and that its pattern of expression is developmentally regulated.

Age Factors↗