The role of ion channels in peripheral sensory neurons in pain and cancer”

Seminar: LIB 110, Nina Boiko, Ph.D., Post-Doc Fellow, UTHSC@San Antonio, TX. “The role of ion channels in peripheral sensory neurons in pain and cancer”.
The transformation of mechanosensory stimuli into changes in sensory neuron activity is incompletely understood. I show that pickpocket1, a Drosophila homolog of mammalian Degenerin/epithelial sodium channels, conducts a depolarizing Na+ current in polymodal multidendritic sensory neurons capable of brining the neuron to threshold and driving action potential firing to affect animal mechanosensitive behaviors. This channel functions as an ionotropic molecular sensory transducer capable of transforming the perception of a stimulus into phasic neuronal activity in peripheral sensory neurons. Using Drosopihla as a model organism I investigated the molecular and cellular underpinnings of chemotherapy-induced peripheral neuropathy (CIPN). CIPN results in profound pain which often constrains use of many important anti-cancer drugs. My hypothesis is that CIPN is a result of prolonged hyperexcitability followed by eventual excitotoxicity. I demonstrate that CIPN results from the direct effects of chemotherapy drugs on peripheral nociceptors and that anti-cancer drugs hyper-excite these neurons by stimulating TrpA1 channels to cause allodynia and hyperalgesia.