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Objective There is evidence that glia-neuron interactions are involved in mechanisms underlying the development of chronic pain.Central sensitization is a state of increased excitability of nociceptive neurons in the spinal dorsal horn following peripheral tissue injury and/or inflammation and is considered a crucial process underlying the development and maintain of chronic pain states.There is growing evidence that astroglia play an important role in chronic pain.Glutamate plays a major role in central sensitization and astrocyte-neuronal glutamate-glutamine cycle is involved in central sensitization in the spinal cord.System A transport is responsible for the accumulation of glutamine by neurons and non-metabolised amino acid analogue α-(methylamino)isobutyric acid (MeAIB) appears to be a specific inhibitor of all isoforms of this transporter.The current study investigated the roles of System A transport in inhibition of central sensitization induced by formalin in rats.Methods A total of 43 male, Sprague Dawley rats, aged 4 months, were randomly assigned to a sham operation group (n =6) and a model group (n =37).Rats in the model group received intrathecal infusion operation at spinal cord.7 days later, 37 model rats were randomly divided into saline, MeAIB 0.05 mM, MeAIB 0.1 mM, MeAIB 0.3 mM, MeAIB 0,5 mM, and MeAIB 1.0 mM and formalin subcutaneous injection alone groups.At 15 min after intrathecal injection, a rat model of formalin-induced inflammatory pain was established by subcutaneous injection of 5% formalin (50 μL) in the left hindpaw.After the completion of behavioral measurements, rats were sacrifice and the spinal cords were removed for GFAP immunohistochemistry staining.Results In this study, intrathecal injection MeAIB produced a dose-dependent inhibition of inflammatory pain, including nociceptive behaviors and GFAP expression in the spinal dorsal horn.In control experiments, intraplantar injection of formalin alone or intrathecal injection of saline did not produce any significant changes in astroglial properties and behavior measurements.Conclusion These findings suggest that system A transport is essential for the initiation of inflammation-induced central sensitization.