Satellite Glial Cells and Neurons in Trigeminal Ganglia Are Altered in an Itch Model in Mice
Itch (pruritus) is a common chronic condition with a lifetime prevalence of over 20%. The mechanisms underlying itch are poorly understood, and its therapy is difficult. There is recent evidence that following nerve injury or inflammation, intercellular communications in sensory ganglia are augmente...
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| Format: | Article |
| Language: | English |
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MDPI AG
2022-03-01
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| Series: | Cells |
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| Online Access: | https://www.mdpi.com/2073-4409/11/5/886 |
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| author | Meytal Cohen Rachel Feldman-Goriachnik Menachem Hanani |
| author_facet | Meytal Cohen Rachel Feldman-Goriachnik Menachem Hanani |
| author_sort | Meytal Cohen |
| collection | DOAJ |
| description | Itch (pruritus) is a common chronic condition with a lifetime prevalence of over 20%. The mechanisms underlying itch are poorly understood, and its therapy is difficult. There is recent evidence that following nerve injury or inflammation, intercellular communications in sensory ganglia are augmented, which may lead to abnormal neuronal activity, and hence to pain, but there is no information whether such changes take place in an itch model. We studied changes in neurons and satellite glial cells (SGCs) in trigeminal ganglia in an itch model in mice using repeated applications of 2,4,6-trinitro-1-chlorobenzene (TNCB) to the external ear over a period of 11 days. Treated mice showed augmented scratching behavior as compared with controls during the application period and for several days afterwards. Immunostaining for the activation marker glial fibrillary acidic protein in SGCs was greater by about 35% after TNCB application, and gap junction-mediated coupling between neurons increased from about 2% to 13%. The injection of gap junction blockers reduced scratching behavior, suggesting that gap junctions contribute to itch. Calcium imaging studies showed increased responses of SGCs to the pain (and presumed itch) mediator ATP. We conclude that changes in both neurons and SGCs in sensory ganglia may play a role in itch. |
| first_indexed | 2024-03-09T20:44:08Z |
| format | Article |
| id | doaj.art-c5c2b8f9f2114a998d129bbeac689425 |
| institution | Directory Open Access Journal |
| issn | 2073-4409 |
| language | English |
| last_indexed | 2024-03-09T20:44:08Z |
| publishDate | 2022-03-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Cells |
| spelling | doaj.art-c5c2b8f9f2114a998d129bbeac6894252023-11-23T22:51:46ZengMDPI AGCells2073-44092022-03-0111588610.3390/cells11050886Satellite Glial Cells and Neurons in Trigeminal Ganglia Are Altered in an Itch Model in MiceMeytal Cohen0Rachel Feldman-Goriachnik1Menachem Hanani2Laboratory of Experimental Surgery, Hadassah-Hebrew University Medical Center, Jerusalem 91240, IsraelLaboratory of Experimental Surgery, Hadassah-Hebrew University Medical Center, Jerusalem 91240, IsraelLaboratory of Experimental Surgery, Hadassah-Hebrew University Medical Center, Jerusalem 91240, IsraelItch (pruritus) is a common chronic condition with a lifetime prevalence of over 20%. The mechanisms underlying itch are poorly understood, and its therapy is difficult. There is recent evidence that following nerve injury or inflammation, intercellular communications in sensory ganglia are augmented, which may lead to abnormal neuronal activity, and hence to pain, but there is no information whether such changes take place in an itch model. We studied changes in neurons and satellite glial cells (SGCs) in trigeminal ganglia in an itch model in mice using repeated applications of 2,4,6-trinitro-1-chlorobenzene (TNCB) to the external ear over a period of 11 days. Treated mice showed augmented scratching behavior as compared with controls during the application period and for several days afterwards. Immunostaining for the activation marker glial fibrillary acidic protein in SGCs was greater by about 35% after TNCB application, and gap junction-mediated coupling between neurons increased from about 2% to 13%. The injection of gap junction blockers reduced scratching behavior, suggesting that gap junctions contribute to itch. Calcium imaging studies showed increased responses of SGCs to the pain (and presumed itch) mediator ATP. We conclude that changes in both neurons and SGCs in sensory ganglia may play a role in itch.https://www.mdpi.com/2073-4409/11/5/886sensory ganglionglial fibrillary acidic proteingap junctioncalcium imagingpurinergic receptor |
| spellingShingle | Meytal Cohen Rachel Feldman-Goriachnik Menachem Hanani Satellite Glial Cells and Neurons in Trigeminal Ganglia Are Altered in an Itch Model in Mice Cells sensory ganglion glial fibrillary acidic protein gap junction calcium imaging purinergic receptor |
| title | Satellite Glial Cells and Neurons in Trigeminal Ganglia Are Altered in an Itch Model in Mice |
| title_full | Satellite Glial Cells and Neurons in Trigeminal Ganglia Are Altered in an Itch Model in Mice |
| title_fullStr | Satellite Glial Cells and Neurons in Trigeminal Ganglia Are Altered in an Itch Model in Mice |
| title_full_unstemmed | Satellite Glial Cells and Neurons in Trigeminal Ganglia Are Altered in an Itch Model in Mice |
| title_short | Satellite Glial Cells and Neurons in Trigeminal Ganglia Are Altered in an Itch Model in Mice |
| title_sort | satellite glial cells and neurons in trigeminal ganglia are altered in an itch model in mice |
| topic | sensory ganglion glial fibrillary acidic protein gap junction calcium imaging purinergic receptor |
| url | https://www.mdpi.com/2073-4409/11/5/886 |
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