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Chronic pain is very poorly, if at all, controlled by currently available therapeutics. We believe that the reason for this failure lies, at least in the part, in the fact that clinically available drugs were developed to target neurons. The work of our laboratory has documented that non-neuronal cells called glia (microglia, astrocytes) are critically involved in the initiation and maintenance of chronic pain. Thus our laboratory is focused on understanding what "triggers" glia to become activated so to begin releasing pain-enhancing substances, and how we can intervene with this pathological side of glia so to prevent and control chronic pain. We are actively pursuing pharmacological and gene therapy approaches to suppress glially-driven pain enhancement with the goal of identifying new strategies for controlling such pathological pain processes in people. In addition, our group has recently discovered that clinically relevant opioids also activate glia, again causing them to release pain-enhancing substances. We have now linked such opioid-induced glial activation to the decreased efficacy of acute opioids in suppressing pain and to the phenomena of opioid tolerance and opioid withdrawal. Similar to our goals of controlling glial dysregulation of pain, we similarly seek to understand how to control the negative impact that glial activation has on opioid analgesia. For both pain and opioid analgesics, the ultimate goal is to find means by which clinical pain control can be improved so to relieve human suffering.