ArticleFrontiers in neurology2026
Kainate-induced ATP release contributes to spinal excitotoxicity that is attenuated by purinergic blockade.
Article in Frontiers in neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Severe spinal cord injury (SCI) is characterized by irreversible neuronal loss and permanent motor/sensory dysfunction with very limited treatment. This study aimed to assess the role of purinergic signalling at a very early stage of SCI following focal chemical injury induced by kainate (KA). Methods: Male and female C57BL/6J and BALB/c mice were used in a SCI model. Real-time biosensor recordings were employed to monitor glutamate and ATP release from spinal tissue under in vitro conditions simulating SCI. Changes in purinergic receptor expression, neuronal survival, glial activation, and locomotor function were evaluated, including the effects of the purinergic antagonist Brilliant Blue G (BBG). Results: KA treatment induced a marked increase in extracellular glutamate and ATP release and significantly elevated mRNA levels of P2X4 and P2X7 receptors. BBG treatment significantly increased neuronal survival compared with KA-treated tissues. No effects on astrocyte or microglial activation were detected at this early stage. In vivo, KA markedly impaired locomotor function, whereas BBG co-treatment produced partial functional recovery. Discussion: These findings support a role for early ATP release in modulating neuronal survival following excitotoxic injury, potentially through CREB-dependent signalling pathways. ATP-dependent mechanisms may therefore represent promising targets for future neuroprotective strategies in SCI.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.