Sensitization induces hypersensitivity in trigeminal nerve.

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.