Effect and mechanism of BDNF/TrkB signaling on vestibular compensation
| Autor: | Dehong Mao, Weichun Li, Linglong Li, Xiaoying Fang, Zhongmei He, Feng Zhang, Wei Xuan, Jiao Deng |
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| Rok vydání: | 2021 |
| Předmět: |
Male
medicine.medical_specialty Time Factors Medial vestibular nucleus Bioengineering Tropomyosin receptor kinase B BDNF/TrkB signaling Applied Microbiology and Biotechnology Rats Sprague-Dawley astrocyte Neurotrophic factors Internal medicine GABAergic neuron medicine Animals Receptor trkB GABAergic Neurons Cell Proliferation vestibular compensation GABAAR Behavior Animal Glial fibrillary acidic protein biology Chemistry Brain-Derived Neurotrophic Factor General Medicine Vestibular nerve Lateral vestibular nucleus medicine.anatomical_structure Endocrinology nervous system Astrocytes biology.protein GABAergic Vestibule Labyrinth TP248.13-248.65 Signal Transduction Research Article Research Paper Biotechnology Astrocyte |
| Zdroj: | Bioengineered article-version (VoR) Version of Record Bioengineered, Vol 12, Iss 2, Pp 11823-11836 (2021) |
| ISSN: | 2165-5987 2165-5979 |
| DOI: | 10.1080/21655979.2021.1997565 |
| Popis: | Brain-derived neurotrophic factor (BDNF) regulates neuronal plasticity by targeting the tyrosine kinase B receptor (TrkB) receptor, but limited researches concentrate on the role of BDNF/TrkB signaling in vestibular compensation. In this study, rats with unilateral vestibular dysfunction were established by unilateral labyrinthectomy (UL) and infusion with siBDNF or 7, 8-Dihydroxyflavone (7,8-DHF, a TrkB receptor agonist). The behavioral scores of rats with vestibular deficits were determined and the rotarod test was performed after UL. BDNF and TrkB levels after UL were determined by western blot and quantitative reverse transcription PCR (qRT-PCR). 5-bromo-2ʹ-deoxyuridine (BrdU)-positive cells (newly generated cells) and GAD67-positive cells (GABAergic neurons) were identified by immunohistochemistry. Glial fibrillary acidic protein (GFAP) (astrocyte marker)-positive cells were identified and GABA type A receptor (GABAAR) expression was detected by immunofluorescence. We found that after UL, BDNF and TrkB levels were up-regulated with a maximum value at 4 h, and then progressively down-regulated during 4 h ~ 7 d. Blocking BDNF/TrkB signaling inhibited the recovery from vestibular deficits, decreased the numbers of newly generated cells and astrocytes in medial vestibular nucleus (MVN), inferior vestibular nerve (IVN), superior vestibular nerve (SVN) and lateral vestibular nucleus (LVN), and disrupted the balances of GABAergic neurons and GABAAR expressions in the left (lesioned) side and right (intact) side of MVN, whereas activation of BDNF/TrkB signaling caused opposite results. The current study indicated that BDNF/TrkB signaling avails vestibular compensation, depending on the number of newly generated cells and astrocytes, the rebalance of GABAergic neurons, and GABAAR expression in bilateral MVN. |
| Databáze: | OpenAIRE |
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