Loss of touch receptors leads to itch Itch in response to light touch of the skin is an aging-associated problem. This phenomenon is called alloknesis and can become a major medical condition associated with dry skin. Feng et al. discovered that loss or dysfunction of Merkel cells causes scratching in mice (see the Perspective by Lewis and Grandl). Reduction of Merkel cell numbers results in reduced firing patterns and frequencies and changes the activation thresholds of slowly adapting afferent nerve fibers. Like hair cells, Merkel cells are lost with age. A painful scratch will temporarily alleviate itch because it induces enough activity through the remaining Merkel cells. Science, this issue p. 530; see also p. 492 Chronic itch caused by aging and dry skin is associated with the loss of skin Merkel cells involved in light touch sensation. The somatosensory system relays many signals ranging from light touch to pain and itch. Touch is critical to spatial awareness and communication. However, in disease states, innocuous mechanical stimuli can provoke pathologic sensations such as mechanical itch (alloknesis). The molecular and cellular mechanisms that govern this conversion remain unknown. We found that in mice, alloknesis in aging and dry skin is associated with a loss of Merkel cells, the touch receptors in the skin. Targeted genetic deletion of Merkel cells and associated mechanosensitive Piezo2 channels in the skin was sufficient to produce alloknesis. Chemogenetic activation of Merkel cells protected against alloknesis in dry skin. This study reveals a previously unknown function of the cutaneous touch receptors and may provide insight into the development of alloknesis.
Piezo2 channel–Merkel cell signaling modulates the conversion of touch to itch
Jing Feng,Jialie Luo,Pu Yang,Junhui Du,Brian S. Kim,Hongzhen Hu
Published 2018 in Science
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- Publication year
2018
- Venue
Science
- Publication date
2018-05-04
- Fields of study
Biology, Medicine
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
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