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<p>This study aimed to characterize peripheral and central sensitization in mechanical allodynia of the tongue induced by sleep-related disorders, neuropathic pain, and inflammatory pain. Male rats were exposed to chronic intermittent hypoxia (CIH) for 16&#xa0;days using an obstructive sleep apnea model. Lingual nerve injury (LNI) was induced to establish a neuropathic tongue pain model, while complete Freund’s adjuvant was injected into the tongue to establish a tongue inflammation (TI) model. The expression levels of calcitonin gene-related peptide (CGRP), hypoxia-inducible factor (HIF)-1α, piezo-type mechanosensitive ion channel component 2 (Piezo2), transient receptor potential cation channel subfamily V member 4 (TRPV4), and glial fibrillary acidic protein (GFAP) in the trigeminal ganglion (TG) and cFos in the trigeminal spinal subnucleus were determined using immunohistochemistry on day 16. All CIH, LNI, and TI rat models exhibited prolonged mechanical allodynia of the tongue. CIH and TI increased the number of CGRP-immunoreactive (IR) neurons and HIF-1α-IR cells. However, only CIH increased the number of Piezo2-IR neurons and GFAP-positive satellite glial cells. The number of TRPV4-IR neurons was elevated in the LNI and TI groups but not in the CIH group. Only CIH induced persistent cFos expression in the trigeminal spinal subnucleus caudalis, indicating long-lasting central sensitization. These findings indicate that CIH-induced tongue pain arises through distinct peripheral and central sensitization processes, highlighting the diverse mechanisms underlying chronic mechanical allodynia of the tongue.</p>

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Involvement of peripheral and central sensitization in prolonged mechanical allodynia of the tongue in a rat

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月25日

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  • Saki Kishimoto,
  • Sho Katsura,
  • Yoshie Okamoto,
  • Hitoshi Niwa,
  • Ayano Katagiri,
  • Takafumi Kato

摘要

This study aimed to characterize peripheral and central sensitization in mechanical allodynia of the tongue induced by sleep-related disorders, neuropathic pain, and inflammatory pain. Male rats were exposed to chronic intermittent hypoxia (CIH) for 16 days using an obstructive sleep apnea model. Lingual nerve injury (LNI) was induced to establish a neuropathic tongue pain model, while complete Freund’s adjuvant was injected into the tongue to establish a tongue inflammation (TI) model. The expression levels of calcitonin gene-related peptide (CGRP), hypoxia-inducible factor (HIF)-1α, piezo-type mechanosensitive ion channel component 2 (Piezo2), transient receptor potential cation channel subfamily V member 4 (TRPV4), and glial fibrillary acidic protein (GFAP) in the trigeminal ganglion (TG) and cFos in the trigeminal spinal subnucleus were determined using immunohistochemistry on day 16. All CIH, LNI, and TI rat models exhibited prolonged mechanical allodynia of the tongue. CIH and TI increased the number of CGRP-immunoreactive (IR) neurons and HIF-1α-IR cells. However, only CIH increased the number of Piezo2-IR neurons and GFAP-positive satellite glial cells. The number of TRPV4-IR neurons was elevated in the LNI and TI groups but not in the CIH group. Only CIH induced persistent cFos expression in the trigeminal spinal subnucleus caudalis, indicating long-lasting central sensitization. These findings indicate that CIH-induced tongue pain arises through distinct peripheral and central sensitization processes, highlighting the diverse mechanisms underlying chronic mechanical allodynia of the tongue.