Abstract

Cellular electrical activity is the result of a highly complex process that involve the activation of ion channel proteins. Ion channels make pores on cell membranes that rapidly transit between conductive and non-conductive states, allowing different ions to flow down their electrochemical gradients across cell membranes. In the case of neuronal cells, ion channel activity orchestrates action potentials traveling through axons, enabling electrical communication between cells in distant parts of the body. Somatic sensation -our ability to feel touch, temperature and noxious stimuli- require ion channels able to sense and respond to our peripheral environment. Sensory integration involves the summing of various environmental cues and their conversion into electrical signals. Members of the Transient Receptor Potential (TRP) family of ion channels have emerged as important mediators of both, cellular sensing and sensory integration. The regulation of the spatial and temporal distribution of membrane receptors is recognized as an important mechanism for controlling the magnitude of the cellular response and the time scale on which cellular signaling occurs. Several studies have shown that this mechanism is also used by TRP channels to modulate cellular response and ultimately fulfill their physiological function as sensors. However, the inner-working of this mode of control for TRP channels remains poorly understood. The question of whether TRPs intrinsically regulate their own vesicular trafficking or weather the dynamic regulation of TRP channel residence on the cell surface is caused by extrinsic changes in the rates of vesicle insertion or retrieval remain open. This review will examine the evidence that sub-cellular redistribution of TRP channels plays an important role in regulating their activity and explore the mechanisms that control the trafficking of vesicles containing TRP channels.

Keywords: TRP channels, traffic, vesicles, regulated exocytosis, Cellular electrical activity, ion channel proteins, Transient Receptor Potential, ansmembrane (TM) monomers, Kv channels, AMPA1, NMDA2, GABA3, ENaC epithelial sodium channel, Aquaporin 2 (AQP2) water channel, TRPML, mucolipin, Varitint-Waddler, ArF6-positive, recycling endosome, heteromultimeric channel complexes, tubulo-vesicular structures, mGluR6-coupled cation, modulated by NAADP, cytosolic ADP-ribose (ADPR), capsaicin receptor, thapsigargin-insensitive store, Ca2+ release-activated, Synaptic Vesicle, ACh-containing vesicles, ion exchange gel theory, Kinase-inactive mutants, PKC9-dependent exocytosis, botulinum neurotoxin, Yeast two-hybrid assays, phorbol ester 4-PDD, Mechanotransduction, Exocytosis, Xenopus oocytes, PACSIN3, Rab Proteins, CLATHRIN-DEPENDENT, Caveolae Related Proteins, Dynamin