Abstract: Pain, as a sub modality of somatic sensation, has been defined as a complex constellation of unpleasant sensory, emotional and cognitive experiences provoked by real or perceived tissue damage and manifested by certain autonomic, psychological, and behavioral reactions. The benefit of these unpleasant sensations, however, is underscored by extreme cases: patients lacking the ability to perceive pain due to hereditary neuropathies often maintain unrealized infections; self mutilate, and have curtailed life spans. Normally, nociception and the perception of pain are evoked only at pressures and temperatures extreme enough to potentially injured tissues and by toxic molecules and inflammatory mediators. As opposed to the relatively more objective nature of other senses, pain is highly individual and subjective and the translation of nociception into pain perception can be curtailed by stress or exacerbated by anticipation (Woolf). Chronic pain is estimated to affect millions of people worldwide and is one of the most common reasons for physician visits (Scascighini et al. 2008). Inflammation may cause direct painful stimuli as well as sensitize nociceptors to stimulation (McMahon et al. 2005). Thus, there are multiple points along the pain pathway that represent opportunities for therapeutic intervention. Despite this, there are only a limited number of mechanisms through which current pain medications work. Major classes of analgesics include opioids, non-steroidal anti-inflammatory drugs, antidepressants, and anticonvulsants. Although these treatments provide relief, the effects are often incomplete and complicated by serious side effects and/or tolerance. Thus, therapeutics with novel mechanisms of actions are desperately needed (Finnerup et al. 2005). What exactly, from a neurobiological perspective, is pain? Pain is actually three quite different things, although it is difficult to make the distinction; nociceptive pain, inflammatory pain and neuropathic pain. Nociceptive pain is not a clinical problem, except in the specific context of surgery and other clinical procedures that necessarily involve noxious stimuli, where it must be suppressed by local and general anesthetics or high-dose opioids (Woolf). Nociception involves multiple steps from the peripheral receptor, the afferent nerve transmitting the impulse to the spinal cord, the signal processing in the dorsal horn, with inhibitory and facilitatory elements and finally transmission to higher cerebral centers where the peripheral nociceptive stimulus is perceived as pain (Arendt-Nielsen and Sumikura 2002). The second kind of pain is also adaptive and protective. By heightening sensory sensitivity after unavoidable tissue damage, this pain assists in the healing of the injured body part by