Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2012
Sensitization induces hypersensitivity in trigeminal nerve.
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Wang X, Liang H, Zhou C, Xu M, Xu L
Аннотация
BACKGROUND AND AIMS: Trigeminal neuralgia is one of the chronic neuropathic pains. The aetiology remains unclear. Chronic inflammation is proposed playing a role in the pathogenesis of trigeminal neuralgia. This study aims to assess the role of allergic inflammation in the pathological status of trigeminal neuralgia.
METHODS: Allergic inflammation was induced in the infraorbital skin of rats. The expression of 5-HT receptor 3 (R3) in the trigeminal nerve and mastocytosis in the local tissue were observed by immunohistochemistry. The hyperalgesia status of the trigeminal nerve was determined by quantitatively recording the head-withdrawal threshold to mechanical stimulation of the infraorbital nerve territory.
RESULTS: After sensitization, the expression of 5-HT R3 in the trigeminal nerve and the frequency of mast cells were markedly increased in the epidermal tissue of the infraorbital area. Applying exogenous 5-HT to the local tissue also increased the expression of 5-HT R3 in the trigeminal nerve. The threshold of mechanical allodynia to stimuli was significantly lower in sensitized rats than control rats, which could be blocked by pre-treatment with either 5-HT R3 antagonists, or neurokinin-1 antagonists, or mast cell stabilizers.
CONCLUSIONS: Allergic inflammation can induce the overexpression of 5-HT R3 in the trigeminal nerve to induce the hyperalgesia status in the trigeminal nerve. The 5-HT R3 may be a therapeutic target in the treatment of trigeminal neuralgia.
METHODS: Allergic inflammation was induced in the infraorbital skin of rats. The expression of 5-HT receptor 3 (R3) in the trigeminal nerve and mastocytosis in the local tissue were observed by immunohistochemistry. The hyperalgesia status of the trigeminal nerve was determined by quantitatively recording the head-withdrawal threshold to mechanical stimulation of the infraorbital nerve territory.
RESULTS: After sensitization, the expression of 5-HT R3 in the trigeminal nerve and the frequency of mast cells were markedly increased in the epidermal tissue of the infraorbital area. Applying exogenous 5-HT to the local tissue also increased the expression of 5-HT R3 in the trigeminal nerve. The threshold of mechanical allodynia to stimuli was significantly lower in sensitized rats than control rats, which could be blocked by pre-treatment with either 5-HT R3 antagonists, or neurokinin-1 antagonists, or mast cell stabilizers.
CONCLUSIONS: Allergic inflammation can induce the overexpression of 5-HT R3 in the trigeminal nerve to induce the hyperalgesia status in the trigeminal nerve. The 5-HT R3 may be a therapeutic target in the treatment of trigeminal neuralgia.