Keratinocytes can modulate and directly initiate nociceptive responses
Year: 2015
Type: article
Abstract: How thermal, mechanical and chemical stimuli applied to the skin are transduced into signals transmitted by peripheral neurons to the CNS is an area of intense study. Several studies indicate that transduction mechanisms are intrinsic to cutaneous neurons and that epidermal keratinocytes only modulate this transduction. Using mice expressing channelrhodopsin (ChR2) in keratinocytes we show that blue light activation of the epidermis alone can produce action potentials (APs) in multiple types of cutaneous sensory neurons including SA1, A-HTMR, CM, CH, CMC, CMH and CMHC fiber types. In loss of function studies, yellow light stimulation of keratinocytes that express halorhodopsin reduced AP generation in response to naturalistic stimuli. These findings support the idea that intrinsic sensory transduction mechanisms in epidermal keratinocytes can directly elicit AP firing in nociceptive as well as tactile sensory afferents and suggest a significantly expanded role for the epidermis in sensory processing.
Source: eLife
DOI: 10.7554/elife.09674
Language: English
Topic: Ion Channels and Receptors
Subfield: Sensory Systems
Field: Neuroscience
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $2,500
Awards: Peripheral Nerve Regeneration and Sensory Neuron Plasticity, Effects of Artemin on Nociceptors, Phenotyping pain in a mouse model of pancreatic cancer, Characterization of epithelial-neural communication, Optogenetic dissection of the functional properties of bladder afferent populations, Digestive Diseases Training Program, University of Pittsburgh Clinical and Translational Science Institute, Peripheral Nerve Regeneration and Sensory Neuron Plasticity, Characterization and Plasticity of Visceral Nociceptors, Optogenetic analysis of epidermal-neuronal interaction, G857490982, G9000201226, Investigating the Neural Circuits of Itch, Training in Mechanisms and Clinical Presentation of Pain
OpenAlex ID: W2177347011
