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We postulate that early and repeated exposure to endothelin-1, as occurs during a sickle cell episode, sensitizes the organism thus, producing greater pain responses upon subsequent exposure, decreasing opioid analgesia, and producing a vulnerability to seek psychoactive drugs but may protect from the escalation of psychoactive drugs and resultant addiction. Understanding the mechanisms that underlie these changes will identify novel molecular targets for the treatment of pain during sickle cell episodes as they occur across the life-span.

With estimates of fetal alcohol exposure ranging from 1-10 in 1000 births it is important to assess whether alterations in pain processing are a part of fetal alcohol spectrum disorder. Adolescents make up a second vulnerable population with over 80% of high school students having consumed alcohol by the time of graduation. With pain being the most common reason patients seek medical care an understanding of how alcohol exposure during development may impact pain sensation and analgesia is critical to provide adequate pain control to alcohol-exposed patients.

The mechanisms underlying neuropathic pain states are not completely understood, and the use of systemic opioids, however, is limited by their central nervous system side effects, e.g., sedation and cognitive dysfunction. These studies overexpress opioid receptors in primary afferents by topical administration of viral constructs as a strategy for the treatment of neuropathic pain.

Understanding how opioid exposure in infancy impacts pain and analgesia throughout development

Optimizing neuronal growth in collagen tubes

School of Medicine:
Dr. Stephen Fann
Dr. Michael Yost
Dr. Carla Roberts
Dr. Steven Wilson
Dr. L. Britt Wilson
Dr. Kenneth Walsh

Psychology:
Dr. Jeffrey Schatz
Dr. Catherine McClellan
Dr. Sandra Kelly