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Full list of author information is available at the end of the articleBackground The processing of sensory information from primary afferent neurons to the spinal dorsal horn may change significantly following tissue inflammation, ultimately leading to the development of chronic pain. Abnormal pain manifestations, such as allodynia, hyperalgesia, and spontaneous pain episodes occurring in these patho-logical pain states, are believed to result, at least in part, from plasticity phenomena in the spinal sensory system [1,2]. Functional alterations in the properties of Aβ pri-mary afferents may notably account for the increased pain sensitivity observed under peripheral chronic inflam-mation. Variations in neurotransmitter content and release, changes in membrane receptor function and trafficking, and regulation of ion channel expression and activity may indeed enhance the excitability of Aβ-fibers and thus contribute t