Activity-Dependent Plasticity in Sensory Neurons: From TRPV1 to NFAT
Wednesday -
May 14, 2008
07-08 SEMINAR SERIES
Yuriy Usachev
Assistant Professor University of Iowa, Carver College of Medicine
Speaker's website
Host: Santana
Primary nociceptors are specialized sensory neurons that detect and signal potentially damaging environmental conditions, such as extreme heat or cold, exposure to chemical irritants or the presence of sharp objects. Sensitization and increased excitability of primary nociceptors triggered by injury or illness are thought to be central for the development of inflammatory and neuropathic pain. We are using molecular, genetic and electrophysiological approaches in combination with behavioral studies to dissect the mechanisms that underlie activity-dependent plasticity in nociceptors. The first part of my talk will focus on the function and modulation of the vanilloid receptor TRPV1, which is postulated to serve as a molecular detector of noxious heat in nociceptors. I will describe our recent findings on the role of the scaffolding protein AKAP150 in the regulation of TRPV1 function and TRPV1-mediated thermal hyperalgesia. In the second part of my talk, I will share our recent data on the regulation of the Ca2+-dependent transcription factor NFAT in sensory neurons by electrical activity, TRPV1 agonists and nerve growth factor (NGF). Our findings suggest that NFAT serves as an integrator of electrical activity and neurotrophin signaling to trigger a specific transcriptional response in neurons.