Radicular pain can be caused by a disc herniation that can compress the spinal nerve roots as they exit the spinal canal [1]. Pain models in the rat mimic both the mechanical and chemical components of a disc herniation, either individually or in combination, and have demonstrated that the specific injury inputs (i.e. mechanics, inflammation) modulate the pain responses [2,3]. For both types of nerve root injuries, allodynia (i.e. pain) is elevated as early as 1 day after injury but its temporal responses vary over time according to the type of injury insult [3]. Painful nerve root injuries also induce a host of inflammatory cascades in the spinal cord that promote neuronal healing [2–4]. Although inflammatory responses have been shown to relate to the onset and maintenance of pain following injury, the specific biochemical processes and their relationship to inflammation and pain symptoms are not yet fully defined.

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