Abstract
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.
Highlights
To explore the possible role of satellite glial cells (SGCs) in pruritus, we investigated, in this model, how neurons and SGCs in the mouse trigeminal ganglion (TG) were altered
We examined dye coupling between cells in TG from TNCB-treated mice
On Day 14 of the TNCB protocol, the number of TG neurons surrounded by GFAP-positive SGCs was greater by about 35% than that of controls
Summary
Itch (pruritus) has been defined as “an unpleasant cutaneous sensation that provokes the desire to scratch” [1]. This is a very common chronic condition affecting over 20% of the population during their lifetime [2], and it is difficult to treat [3–5]. Pruritus is associated with many skin diseases, the most prevalent of which is atopic dermatitis [6]. Pruritus is frequently present in systemic disease (renal, hepatic, and others) and is caused by numerous medications [1]. Pruritus has a major detrimental influence on the quality of life, which is comparable to that of chronic pain, requiring the use of tranquilizers or antidepressants [1,7]. Chronic itch may lead to repetitive scratching that causes skin lesions, which can worsen the itch sensation and lead to further scratching (the itch–scratch cycle)
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