NG2-glia alters its dynamics in response to L-DOPA-induced dyskinesia. In these animals, striatal NG2-glia density was reduced with cells presenting activated phenotype while doxycycline antidyskinetic therapy promotes a return to NG2-glia cell density and protein to a not activated state.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10084551PMC
http://dx.doi.org/10.1177/17590914231155976DOI Listing

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NG2-glia alters its dynamics in response to L-DOPA-induced dyskinesia. In these animals, striatal NG2-glia density was reduced with cells presenting activated phenotype while doxycycline antidyskinetic therapy promotes a return to NG2-glia cell density and protein to a not activated state.

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Neuron-glia antigen 2 (NG2) proteoglycan and platelet-derived growth factor receptor beta (PDGFR-β) are widely used markers of pericytes, which are considered cells that form fibrotic scars in response to central nervous system insults. However, the exact phenotypes of NG2- and PDGFR-β-expressing cells, as well as the origin of the fibrotic scar after central nervous system insults, are still elusive. In the present study, we directly examined the identities and distributions of NG2- and PDGFR-β-positive cells in the control and lesioned striatum injured by the mitochondrial toxin 3-nitropropionic acid.

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Sci Rep

October 2020

Programa de Pós-Graduação em Biociências, Universidade Federal de Ciências da Saúde de Porto Alegre (UFCSPA), Porto Alegre, RS, 90170-050, Brazil.

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Our aim was to examine the spatiotemporal profiles and phenotypic characteristics of neuron-glia antigen 2 (NG2) glia and their associations with neuroglial cells in striatal lesions due to the mitochondrial toxin 3-nitropropionic acid (3-NP). In control striatum, weak NG2 immunoreactivity was restricted to resting NG2 glia with thin processes, but prominent NG2 expression was noted on activated microglia/macrophages, and reactive NG2 glia in the lesion core after 3-NP injection. Activation of NG2 glia, including enhanced proliferation and morphological changes, had a close spatiotemporal relationship with infiltration of activated microglia into the lesion core.

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Department of Experimental Medical Science, Wallenberg Neuroscience Center, Lund University, 221 84 Lund, Sweden; Lund Stem Cell Center, Lund University, 221 84 Lund, Sweden. Electronic address:

The possibility of directly converting non-neuronal cells into neurons in situ in the brain would open therapeutic avenues aimed at repairing the brain after injury or degenerative disease. We have developed an adeno-associated virus (AAV)-based reporter system that allows selective GFP labeling of reprogrammed neurons. In this system, GFP is turned on only in reprogrammed neurons where it is stable and maintained for long time periods, allowing for histological and functional characterization of mature neurons.

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