ABSTRACT
Chronic pain affects the lives of millions of people, and its treatment remains one of the most challenging problems faced by clinicians who can offer their patients few if any effective means of relief devoid of serious side effects. Chronic pain commonly arises following injury to the peripheral nervous system, and this is termed neuropathic pain. A major problem in developing effective treatments for chronic neuropathic pain lies in the translation of basic science research using animal models to the clinic. The consensus arising from both clinical and preclinical data is that peripheral neuropathic pain reects aberrant activity in subsets of primary afferent neurons. However, there is little agreement on which subpopulations are responsible for each and/or all aspects of neuropathic pain, which afferents are necessary for the initiation of neuropathic pain, and whether the same afferents continue to play the same role over time. The unraveling of neuropathic pain requires the development of new approaches that allow investigators to selectively identify and modulate activity in specic subsets of sensory neurons believed to be involved in this process. Here we will discuss recent developments in our understanding of possible molecular mechanisms involved in modulation of primary sensory neuron function and new experimental methods for investigating unique subsets. In addition, we will discuss similarities in sensory neurons across species and the parallel changes in function observed in animal models and human pain disorders.
