ArticleJournal of molecular neuroscience : MN2012
Blockade of P2 nucleotide receptors after spinal cord injury reduced the gliotic response and spared tissue.
Article in Journal of molecular neuroscience : MN, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Inhibition of the P2Y2 Receptor Promotes Facial Nerve Function by Enhancing Neuron Autophagy.Current neuropharmacology · 2026Article
- The role of purinergic receptors in neural repair and regeneration after spinal cord injury.Neural regeneration research · 2023Review
- MicroRNA: Crucial modulator in purinergic signalling involved diseases.Purinergic signalling · 2023Review
- Corrigendum: Purinergic signaling systems across comparative models of spinal cord injury.Neural regeneration research · 2023Article
- Purinergic signaling systems across comparative models of spinal cord injury.Neural regeneration research · 2022Review
- P2Y2 Receptor Mediated Neuronal Regeneration and Angiogenesis to Affect Functional Recovery in Rats with Spinal Cord Injury.Neural plasticity · 2022Article
- Diadenosine tetraphosphate (ApPurinergic signalling · 2017Article
- Purinergic Modulation of Spinal Neuroglial Maladaptive Plasticity Following Peripheral Nerve Injury.Molecular neurobiology · 2015Article
- Antagonism of purinergic signalling improves recovery from traumatic brain injury.Brain : a journal of neurology · 2013Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Spinal cord injury (SCI) triggers a sequel of events commonly associated with cell death and dysfunction of glias and neurons surrounding the lesion. Although astrogliosis and glial scar formation have been involved in both damage and repair processes after SCI, their role remains controversial. Our goal was to investigate the effects of the P2 receptors antagonists, PPADS and suramin, in the establishment of the reactive gliosis and the formation of the glial scar. Molecular biology, immunohistochemistry, spared tissue, and locomotor behavioral studies were used to evaluate astrogliosis, in adult female Sprague-Dawley rats treated with P2 antagonists after moderate injury with the NYU impactor device. Semi-quantitative RT-PCR confirmed the presence of P2Y(1,) P2Y(2,) P2Y(4,) P2Y(6,) P2Y(12), and P2X(2) receptors in the adult spinal cord. Immunohistochemistry studies confirmed a significant decrease in GFAP-labeled cells at the injury epicenter as well as a decrease in spared tissue after treatment with the antagonists. Functional open field testing revealed no significant locomotor score differences between treated and control animals. Our work is consistent with studies suggesting that astrogliosis is an important event after SCI that limits tissue damage and lesion spreading.
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Registered trials
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