We've updated our Privacy Policy to make it clearer how we use your personal data.

We use cookies to provide you with a better experience. You can read our Cookie Policy here.

Advertisement
The Molecular Basis of an Itch
News

The Molecular Basis of an Itch

The Molecular Basis of an Itch
News

The Molecular Basis of an Itch

Credit: Pixabay
Read time:
 

Want a FREE PDF version of This News Story?

Complete the form below and we will email you a PDF version of "The Molecular Basis of an Itch"

First Name*
Last Name*
Email Address*
Country*
Company Type*
Job Function*
Would you like to receive further email communication from Technology Networks?

Technology Networks Ltd. needs the contact information you provide to us to contact you about our products and services. You may unsubscribe from these communications at any time. For information on how to unsubscribe, as well as our privacy practices and commitment to protecting your privacy, check out our Privacy Policy

A new study of male mice published in JNeurosci uncovers two distinct pathways through which a single molecule can cause both itchy and painful skin. The research could inform the development of drugs for a variety of skin diseases.

Diana Bautista and colleagues show that sphingosine 1-phosphate (S1P) — a molecule implicated in skin conditions such as psoriasis as well as other inflammatory diseases including asthma and multiple sclerosis — triggers itch in addition to its known role in pain. Their work identifies a receptor of this molecule, S1PR3, expressed in sensory neurons is responsible for these sensations. The findings suggest that blocking this receptor may represent a promising therapeutic approach for managing both pain and itch.

This article has been republished from materials provided by SfN. Note: material may have been edited for length and content. For further information, please contact the cited source.


Reference:
Hill, R., Morita, T., Brem, R., & Bautista, D. (2018). S1PR3 mediates itch and pain via distinct TRP channel-dependent pathways. The Journal Of Neuroscience, 1266-18. doi: 10.1523/jneurosci.1266-18.2018

Advertisement