Inflammatory pain comprises bidirectional communication between the immune and nervous system that results in a myriad of changes within the somatosensory system. This results in amplified transmission of nociceptive signals and the unmasking of neural circuits that enable innocuous stimuli to drive central pain circuitry following injury. With increasing use of techniques to genetically ablate or manipulate molecularly defined neuronal subtypes our understanding of nociceptor plasticity mechanisms and the spinal and supraspinal circuits that are recruited is rapidly expanding. Here this inflammatory neural plasticity is reviewed, highlighting recent insights that shed light upon nociceptor and central mechanisms that promote hyperalgesia and also the central unmasking of allodynia circuitry.