Abstract: Chronic pain is sustained by a phenomenon of hyper-activation of nociceptive neurons both at peripheral (peripheral sensitization) and central (central sensitization) levels. The onset and maintenance of pain, however, is to be found in the interaction among the various cell populations in the nervous tissue including neurons and glia (Nam et al., 2016). The pathogenesis of neuropathic pain is extremely complex depending on the primary cause of nerve damage, e.g. traumatic nerve injury is associated with a robust inflammatory response while chemotherapy-induced pain is characterized by a modest phlogistic component (Di Cesare Mannelli et al., 2013). Despite these differences, a powerful common concept to explain the cellular mechanisms underlying pain is the activation of glia. The existence of a causal relationship between glia response and pain has been amply demonstrated starting from the mid 1990s (Colburn RW et al., 1999). During the development of neuropathy, a pivotal role has been imputed to microglia, whereas astrocytes are involved in the chronicization of pain (Scholz et al., 2007).