Targeted inhibition of the BDNF/AKT/mTOR pathway in the inferior colliculus ameliorates salicylate-induced tinnitus in rats.

Jiachuan Lin, Jiaqian Wu, Yingxin Wang, Yan Huo, Jianning Zhang

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Article in iScience, 2026. 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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5 authors.

Jiachuan LinDepartment of Otolaryngology, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.

Jiaqian WuDepartment of Otolaryngology, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.

Yingxin WangDepartment of Otolaryngology, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.

Yan HuoDepartment of Otolaryngology, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.

Jianning ZhangDepartment of Otolaryngology, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.

Funding

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6 · The paper itself

Abstract

Tinnitus involves peripheral auditory damage and aberrant central plasticity, with dysregulated BDNF signaling linking injury to compensation. Yet, direct evidence connecting BDNF/AKT/mTOR pathway activation to behavioral phenotypes is limited. This study examined BDNF/AKT/mTOR expression in the inferior colliculus (IC) of sodium salicylate (SS)-induced tinnitus rats and assessed therapeutic inhibition. Rats received intraperitoneal SS, showing decreased GPIAS ratios, elevated ABR thresholds, and upregulated BDNF/TrkB/AKT/mTOR phosphorylation in the IC-changes associated with tinnitus-like behavior. Bilateral IC microinjection of BDNF siRNA or systemic rapamycin revealed that siRNA suppressed BDNF/TrkB and ameliorated tinnitus without improving hearing, while rapamycin reduced mTOR phosphorylation and partially alleviated behavior. These results first demonstrate that BDNF/AKT/mTOR upregulation in the IC contributes to tinnitus in SS rats, and its inhibition improves behavioral manifestations without reversing peripheral hearing loss.

Indexed as

BDNFinferior colliculusmTORsodium salicylatetinnitus

Identifiers

PMID42592457

DOI10.1016/j.isci.2026.117102

PMCPMC13463972

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