Envolvimento das células da glia na ação antinociceptiva da toxina phα1β e da ω-conotoxina mviia na dor inflamatória periférica

Abstract

A peripheral inflammatory injury increases the mechanical sensitivity in response to light-touch, also named as allodynia. The discovery that spinal astrocytes and microglia become reactive to the peripheral inflammation suggests that the glia presumably engage with the pain pathophysiology. Here, we found that the peripheral inflammation induced by intraplantar injection of complete Freund’s adjuvant (CFA) produce mechanical allodynia and robust changes in the spinal glial. Among these changes we found an increase of specific glial markers, increment of astrocytes proliferation, elevation of microglia density and morphologic changes, all of them compatible with the glia reactive phenotype. Moreover, we found that intrathecal injection with the analgesic Phα1β spider toxin, a voltage-gated calcium channel (VGCC) blocker, reverses all the glial pathological features of the peripheral inflammation. We therefore suggest that the Phα1β toxin, apart from its notable analgesic effects, is also a potent anti-inflammatory compound acting on glial plasticity.