ArticleMolecular pain
Bradykinin B2 receptor triggers ITPR1-Mediated ER calcium release in trigeminal ganglion neurons to drive trigeminal neuropathic pain.
Article in Molecular pain. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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9 authors.
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Abstract
ObjectiveTo elucidate the role and underlying mechanism of bradykinin (BK) B2 receptor and its downstream inositol 1,4,5-trisphosphate receptor type 1 (ITPR1)-mediated endoplasmic reticulum (ER) calcium release signaling in the development and maintenance of trigeminal neuropathic pain.MethodsA partial infraorbital nerve transection (pIONT) mouse model of trigeminal neuralgia was employed. Mechanical allodynia was assessed using von Frey filaments. The expression and localization of BK, B2 receptor, and related molecules in the trigeminal ganglion (TG) were analyzed by quantitative real-time PCR (qPCR), Western blot, and immunofluorescence staining. Whole-cell patch-clamp recordings were performed to evaluate TG neuronal excitability. Intracellular calcium signals induced by BK were monitored through Fluo-4 AM calcium imaging. Pharmacological and genetic interventions were conducted via local TG injection of B2 receptor antagonist Icatibant, ITPR1 inhibitor 2-APB, and
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