دورية أكاديمية
S1PR3 Mediates Itch and Pain via Distinct TRP Channel-Dependent Pathways.
| العنوان: | S1PR3 Mediates Itch and Pain via Distinct TRP Channel-Dependent Pathways. |
|---|---|
| المؤلفون: | Hill RZ; Department of Molecular and Cell Biology., Morita T; Department of Molecular and Cell Biology., Brem RB; Department of Plant and Microbial Biology.; Buck Institute for Research on Aging, Novato, California 94945., Bautista DM; Department of Molecular and Cell Biology, dbautista@berkeley.edu.; Helen Wills Neuroscience Institute, University of California, Berkeley, California 94720, and. |
| المصدر: | The Journal of neuroscience : the official journal of the Society for Neuroscience [J Neurosci] 2018 Sep 05; Vol. 38 (36), pp. 7833-7843. Date of Electronic Publication: 2018 Aug 06. |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: Society for Neuroscience Country of Publication: United States NLM ID: 8102140 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1529-2401 (Electronic) Linking ISSN: 02706474 NLM ISO Abbreviation: J Neurosci Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: Washington, DC : Society for Neuroscience Original Publication: [Baltimore, Md.] : The Society, c1981- |
| مواضيع طبية MeSH: | Lysophospholipids/*metabolism , Pain/*metabolism , Pruritus/*metabolism , Receptors, Lysosphingolipid/*metabolism , Signal Transduction/*physiology , Sphingosine/*analogs & derivatives , TRPV Cation Channels/*metabolism, Animals ; Calcium/metabolism ; Mice ; Mice, Knockout ; Pain/genetics ; Pruritus/genetics ; Receptors, Lysosphingolipid/genetics ; Sphingosine/metabolism ; Sphingosine-1-Phosphate Receptors ; TRPV Cation Channels/genetics |
| مستخلص: | Sphingosine 1-phosphate (S1P) is a bioactive signaling lipid associated with a variety of chronic pain and itch disorders. S1P signaling has been linked to cutaneous pain, but its role in itch has not yet been studied. Here, we find that S1P triggers itch and pain in male mice in a concentration-dependent manner, with low levels triggering acute itch alone and high levels triggering both pain and itch. Ca 2+ imaging and electrophysiological experiments revealed that S1P signals via S1P receptor 3 (S1PR3) and TRPA1 in a subset of pruriceptors and via S1PR3 and TRPV1 in a subset of heat nociceptors. Consistent with these findings, S1P-evoked itch behaviors are selectively lost in mice lacking TRPA1, whereas S1P-evoked acute pain and heat hypersensitivity are selectively lost in mice lacking TRPV1. We conclude that S1P acts via different cellular and molecular mechanisms to trigger itch and pain. Our discovery elucidates the diverse roles that S1P signaling plays in somatosensation and provides insight into how itch and pain are discriminated in the periphery. SIGNIFICANCE STATEMENT Itch and pain are major health problems with few effective treatments. Here, we show that the proinflammatory lipid sphingosine 1-phosphate (S1P) and its receptor, S1P receptor 3 (S1PR3), trigger itch and pain behaviors via distinct molecular and cellular mechanisms. Our results provide a detailed understanding of the roles that S1P and S1PR3 play in somatosensation, highlighting their potential as targets for analgesics and antipruritics, and provide new insight into the mechanistic underpinnings of itch versus pain discrimination in the periphery. (Copyright © 2018 the authors 0270-6474/18/387833-11$15.00/0.) |
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| معلومات مُعتمدة: | T32 GM007232 United States GM NIGMS NIH HHS |
| فهرسة مساهمة: | Keywords: GPCR; TRP channel; itch; nociception; pain; sphingosine 1-phosphate |
| المشرفين على المادة: | 0 (Lysophospholipids) 0 (Receptors, Lysosphingolipid) 0 (S1pr3 protein, mouse) 0 (Sphingosine-1-Phosphate Receptors) 0 (TRPV Cation Channels) 0 (TRPV1 protein, mouse) 26993-30-6 (sphingosine 1-phosphate) NGZ37HRE42 (Sphingosine) SY7Q814VUP (Calcium) |
| تواريخ الأحداث: | Date Created: 20180808 Date Completed: 20191015 Latest Revision: 20191210 |
| رمز التحديث: | 20231215 |
| مُعرف محوري في PubMed: | PMC6125817 |
| DOI: | 10.1523/JNEUROSCI.1266-18.2018 |
| PMID: | 30082422 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 1529-2401 |
|---|---|
| DOI: | 10.1523/JNEUROSCI.1266-18.2018 |