My research goal is to identify novel therapeutic interventions for pain that lack abuse liability and adverse side-effects. I lead a multidisciplinary research team that combines approaches from behavioral pharmacology, drug abuse, neurophysiology, neuroanatomy, biochemistry and molecular biology. My research has focused on harnessing the therapeutic potential of cannabinoid signaling systems while minimizing unwanted side effects (i.e. psychoactivity and addiction). The endocannabinoid system consists of cannabinoid receptors (CB1 and CB2), endogenous ligands (endocannabinoids) and the enzymes catalyzing endocannabinoid synthesis and degradation. My graduate work first demonstrated that cannabinoids suppress activity in nociceptive neurons. My postdoctoral work mapped locations and phenotypes of cells expressing cannabinoid receptors/mRNA. My lab identified an enzyme (i.e. monoacylglycerol lipase) implicated in endocannabinoid deactivation as a previously unrecognized therapeutic target for pain and stress disorders. We showed that CB2 receptor activation suppressed the processing of pathological pain and validated CB2 receptors as an analgesic target. These studies showed superior therapeutic efficacy of CB2 agonists compared to alternatives in models of chemotherapy-induced neuropathy. We developed rodent models of chemotherapy-induced peripheral neuropathy and used them to validate therapeutic targets. My preclinical work translated to a clinical trial for cannabinoids in chemotherapy induced peripheral neuropathy. Our studies use behavioral, pharmacological, and genetic models as well as biochemical assays, primary neuronal culture, neuroanatomical and in vivo studies to validate therapeutic targets.
Fellowship - NIMH, National Institutes of Health, Bethesda, MD 09/1998
Ph.D. - Brown University, Providence, RI 09/1996
Fellowship - NIDCR, National Institutes of Health, Bethesda, MD 06/1999
ScM - Brown University, Providence, RI 05/1992
