Chronic Pain
Identifying druggable mechanisms that drive persistent pain states
Chronic pain reflects changes across sensory neurons, immune signaling pathways, and central neural circuits. Our laboratory studies the molecular mechanisms that produce tactile and thermal hypersensitivity as well as functional deficits, with an emphasis on pathways that can be pharmacologically targeted without the liabilities of existing analgesics.
We integrate behavioral measures of nociception with lipidomic, peptidomic, and cell-based pharmacology approaches to identify disease-associated signals and determine how they influence pain-transmitting systems. Candidate mechanisms are evaluated using pharmacological and molecular tools to distinguish correlation from causal function.
This work is closely connected to our alcohol research because pain can emerge during withdrawal and may contribute to continued drinking or relapse. Studying this intersection provides opportunities to identify mechanisms and treatments relevant to both chronic pain and addiction.