Mol Pain
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Schwann cells are components of the peripheral nerve myelin sheath, which supports and nourishes axons. Upon injury of the trigeminal nerve, Schwann cells are activated and cause trigeminal neuralgia by engulfing the myelin sheath and secreting various neurotrophic factors. ⋯ Here, we briefly describe the development and activation of Schwann cells after nerve injury. Moreover, we expound on the occurrence, regulation, and treatment of trigeminal neuralgia; further, we point out the current research deficiencies and future research directions.
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Transient receptor potential ankyrin 1 (TRPA1) is well documented as an important molecule in pain hypersensitivity following inflammation and nerve injury and in many other cellular biological processes. Here, we show that TRPA1 is expressed not only by sensory neurons of the dorsal root ganglia (DRG) but also in their adjacent satellite glial cells (SGCs), as well as nonmyelinating Schwann cells. TRPA1 immunoreactivity is also detected in various cutaneous structures of sensory neuronal terminals, including small and large caliber cutaneous sensory fibers and endings. ⋯ SGCs and neurons harvested from DRG proximal to painful tissue inflammation induced by plantar injection of complete Freund's adjuvant show greater AITC-evoked elevation of [Ca2+]i and slower recovery compared to sham controls. Similar TRPA1 sensitization occurs in both SGCs and neurons during neuropathic pain induced by spared nerve injury. Together, these results show that functional TRPA1 is expressed by sensory ganglia SGCs, and TRPA1 function in SGCs is enhanced after both peripheral inflammation and nerve injury, and suggest that TRPA1 in SGCs may contribute to inflammatory and neuropathic pain.