Frontiers in neurology · 2026
Kainate-induced ATP release contributes to spinal excitotoxicity that is attenuated by purinergic blockade.
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Zylberberg Benjamín, Coronel M Florencia, Mazzone Graciela L
Аннотация
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.
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.