Pulp inflammation induces Kv1.1 K+ channel down‐regulation in rat thalamus. (19th April 2021)

• Record Type: Journal Article
• Authors: Murano, Hiroki; Kaneko, Tomoatsu; Zaw, Su Yee Myo; Sone, Phyo Pyai; Zaw, Zar Chi Thein; Okada, Yamato; Sunakawa, Mitsuhiro; Katsube, Ken‐ichi; Okiji, Takashi
• Is Part Of: Oral diseases. Volume 28:Number 6(2022)
• Page Start: 1674
• Page End: 1681
• Publication Date: 2021-04-19
• Subjects: central sensitization -- potassium voltage‐gated channel subfamily A member 1 -- pulp inflammation -- thalamus; Mouth -- Diseases -- Research -- Periodicals; 617.522
• DOI: 10.1111/odi.13866
• Languages: English
• ISSNs: 1354-523X

Abstract

Abstract: Objectives: Signals from inflamed tooth pulp activate thalamic neurons to evoke central sensitization. We aimed to gain insights into the mechanisms mediating the early phase of pulpal inflammation‐induced thalamic neural and glial activation. Materials and Methods: Pulpal inflammation was induced via the application of mustard oil (MO) to the upper first molar of Wistar rats with local anesthesia (LA) or saline injection. After 0.5, 1, 2, and 24 hr, contralateral thalami were subjected to microarrays, a real‐time polymerase chain reaction and immunohistochemistry to identify differentially expressed genes and assess potassium voltage‐gated channel subfamily A member 1 (Kv1.1)‐expressing axons and glial fibrillary acidic protein (GFAP)‐expressing astrocytes. Results: The Kv1.1 gene ( Kcna1 ) was down‐regulated and the density of Kv1.1‐expressing axons decreased in non‐anesthetized rats, but not in anesthetized rats 1 hr after the MO treatment. The density of GFAP‐expressing astrocytes increased in both groups until 24 hr after the MO treatment, with a greater increase being observed in the saline‐injection group than in the LA group. Conclusions: MO induced the transient down‐regulation of Kcna1, transiently reduced the density of Kv1.1‐expressing axons, and increased astrocytes in thalami within 1 hr of pulpal application. These results suggest central sensitization represented by neuronal hyperexcitability and astrocyte activation.