Abstract
Administration of chemicals (pruritogens) into the skin evokes itch based on signal transduction mechanisms that generate action potentials mainly in mechanically sensitive and insensitive primary afferent C-fibers (pruriceptors). These signals from peripheral neurons are processed in spinal and supra-spinal centers of the central nervous system and finally generate the sensation of itch. Compared to chemical stimulation, electrical activation of pruriceptors would allow for better temporal control and thereby a more direct functional assessment of their activation. Here, we review the electrical stimulation paradigms which were used to evoke itch in humans in the past. We further evaluate recent attempts to explore electrically induced itch in atopic dermatitis patients. Possible mechanisms underlying successful pruritus generation in chronic itch patients by transdermal slowly depolarizing electrical stimulation are discussed.
Highlights
L thickening, especially prevalent in eczematous AD skin, adds an additional layer of complexity as it might increase the distance between the most superficial nerve fibers and the transdermal stimulation electrodes as well as the length and axonal branching pattern of the nerve terminals, both of which might influence their excitability [65, 66]. b) Most ion channels with established roles in the transduction of natural nociceptive stimuli, including the polymodal transient receptor potential (TRP) superfamily members TRP vanilloid 1 (TRPV1) and ankyrin 1 (TRPA1), are only weakly voltage dependent, limiting their contribution to electrically induced depolarization [67, 68]
Excitability of sensory nerves to transdermal electrical stimulation depends—in principle—on three major cellular characteristics of a given nerve fiber: (a) the exact geometry of the nerve ending in the skin; (b) the membrane characteristics determining the extent of local depolarization upon electrical stimulation; (c) the encoding of the depolarization into discharges of single APs or bursts
TRPV1and TRPA1-expression was elevated in eczematous AD skin, an effect attributable to an increased expression per cell, as the number of TRPV1/TRPA1-immunopositive nerve fibers was unchanged [72]
Summary
Department of Experimental Pain Research, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany Reviewed by: Li Hu, Chinese Academy of Sciences (CAS), China Earl Carstens, University of California, Davis, United States Specialty section: This article was submitted to Dermatology, a section of the journal
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
