UCLA Department of Head and Neck Surgery, Los Angeles, CA.
Otol Neurotol. 2024 Mar 1;45(3):326-333. doi: 10.1097/MAO.0000000000004104. Epub 2024 Jan 17.
Brain-derived neurotrophic factor (BDNF) is an important factor in the development and neuroprotection of afferent auditory pathways. In this study, we investigated the expression of BDNF in the afferent auditory pathway after cochlear implantation (CI), hypothesizing that electrical stimulation after CI stimulates BDNF expression in the afferent auditory pathway.
Archival human temporal bones from eight patients with a history of CI and five patients with normal hearing (ages 65-93 years old) were studied. Temporal bone specimens were immunoreacted with rabbit polyclonal antibodies against BDNF and mouse monoclonal antibodies against pan-neurofilaments. In cases of unilateral CI, the BDNF expression was compared with the contralateral unimplanted ear and normal temporal bones without hearing loss.
BDNF immunoreactivity (IR) localized to the spiral ganglion neurons (SGNs) somata and the surrounding satellite cells. BDNF-IR in the spiral ganglia was similar in the apical, middle, and basal hook regions. Neurofilament IR localized to SGN nerve fibers in both implanted and unimplanted cochleae. BDNF-IR in the SGN and satellite cells was significantly increased in the implanted specimens compared with the unimplanted specimens ( p < 0.05) and the normal hearing specimens ( p < 0.05). BDNF-IR expression was similar in the unimplanted cochlea and in the normal cochlea. BDNF protein expression was increased despite complete loss of the organ of Corti hair cells and supporting cells. Even in the cases of CI with a 6-mm first-generation electrode, BDNF expression was upregulated throughout the cochlea.
BDNF expression in the SGN appears to be upregulated by the electrical stimulation from CI. This study provides evidence that the electrical stimulation from CI may stimulate the expression of BDNF, playing a neuroprotective role in the rehabilitation of hearing in the deafened ear.
脑源性神经营养因子(BDNF)是传入听觉通路发育和神经保护的重要因素。在这项研究中,我们假设植入人工耳蜗(CI)后的电刺激会刺激传入听觉通路中的 BDNF 表达,因此研究了 CI 后传入听觉通路中 BDNF 的表达。
研究了 8 例有 CI 病史和 5 例听力正常患者(年龄 65-93 岁)的存档人颞骨。颞骨标本用兔抗 BDNF 多克隆抗体和鼠抗泛神经丝单克隆抗体进行免疫反应。在单侧 CI 的情况下,将 BDNF 表达与对侧未植入耳和无听力损失的正常颞骨进行比较。
BDNF 免疫反应(IR)定位于螺旋神经节神经元(SGN)体和周围的卫星细胞。螺旋神经节中的 BDNF-IR 在顶、中、底钩区域相似。神经丝 IR 定位于植入和未植入耳蜗的 SGN 神经纤维。与未植入标本(p<0.05)和正常听力标本(p<0.05)相比,植入标本中 SGN 和卫星细胞中的 BDNF-IR 明显增加。未植入耳蜗和正常耳蜗中的 BDNF-IR 表达相似。尽管 Corti 毛细胞和支持细胞完全丧失,但 BDNF 蛋白表达仍增加。即使在第一代 6mm 电极的 CI 病例中,整个耳蜗的 BDNF 表达也上调。
SGN 中的 BDNF 表达似乎被 CI 的电刺激上调。本研究提供的证据表明,CI 的电刺激可能刺激 BDNF 的表达,在聋耳的听力康复中发挥神经保护作用。