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Animal models, using experimental peripheral nerve injury, have contributed greatly to the understanding of the spinal pathophysiology associated with neuropathic pain. Nerve injury provokes an initial, transient inflammatory response that involves release of cytokines and growth factors. These substances initiate a series of slowly-developing changes in the spinal cord and primary afferent neurons. These include increased excitability and altered Na+ channel expression in primary afferent fibers, attenuation of GABAergic inhibition and increased excitatory synaptic transmission within the dorsal horn. A better understanding of these processes will lead to rational development of novel therapies. [ABSTRACT FROM AUTHOR]