Peripheral sensitization, chronic pain, and itch.
Primary objective: To investigate the mechanisms by which primary sensory neurons become sensitized and determine whether non-neuronal cells such as keratinocytes modulate neural excitability under painful or itchy conditions.
In these studies we utilize viable human sensory neurons in vitro to determine the preclinical validity of mechanisms of pain and itch transduction identified in animal models. Our approach is to compare neural excitability and morphology, as well as gene and protein expression under naive versus painful or itchy conditions.
This work is funded in part by a NIAMS R21.
Forebrain circuits in pain
Primary objective: To identify the neurons in the forebrain that contribute to the expression of affective and motivational behaviors related to pain.
Pain is a multidimensional phenomenon and requires the organized activity of several neural areas sometimes referred to as the 'pain matrix'. We hypothesize that discriminatory and intensity coding occur in parallel with processing of motivational and affective dimensions of the pain experience. Our goal is to dissect the anatomical and cellular pathways leading to the negative affect associated with pain and learn how to modulate activity selectively within this region for relief of suffering.
This work is funded in part by the American Pain Society, the Rita Allen Foundation, and an NIH/NINDS R01.