Department of Otolaryngology at ukb, Charité Medical School, Berlin, Germany.
J Neurotrauma. 2010 Aug;27(8):1499-507. doi: 10.1089/neu.2009.1246.
Although acoustic overstimulation has a major pathophysiological influence on the inner ear, central components of the auditory pathway can also be affected by noise-induced hearing loss (NIHL). The present study investigates the influence of a noise-induced temporary threshold shift (TTS) and/or permanent threshold shift (PTS) on neuronal cell densities in key structures of the central auditory pathway. Mice were noise-exposed (3 h, 5-20 kHz) at 115 dB sound pressure level (SPL) under anesthesia, and were investigated immediately (TTS group, n = 5) after the exposure, or 1 week later (PTS group, n = 6). Unexposed animals were used as controls (n = 7). Frequency-specific auditory brainstem responses (ABR) were recorded to examine auditory thresholds. Cell density was determined within the dorsal (DCN) and ventral (VCN) cochlear nucleus; the central nucleus of the inferior colliculus (ICC); the dorsal, ventral, and medial subdivisions of the medial geniculate body (MGBd, MGBv, and MGBm); and layer I to VI of the primary auditory cortex (AI I-VI). ABR thresholds were significantly elevated in the TTS group (52-69 dB SPL) and in the PTS group (33-42 dB SPL) compared to controls. There was a significant decrease in cell density only in the VCN of the TTS group (-10%), most likely induced by the acute overstimulation of neurons. Cell density was significantly reduced in all investigated auditory structures at 1 week post-exposure (PTS group), except in layer II of the AI (VCN: -30% and DCN: -30% (high-frequency); -39% (low-frequency); ICC: -31%; MGBd: -31%; MGBm: -28%; MGBv: -31%; AI: -10 to 14%). Thus there were dramatic changes within the neuronal cytoarchitecture of the central auditory pathway following a single noise exposure. The present findings should help clinicians to better understand the complex psychoacoustic phenomena of NIHL.
虽然声过载对内耳有主要的病理生理学影响，但听觉通路的中枢成分也可能受到噪声性听力损失（NIHL）的影响。本研究调查了噪声诱导的暂时阈移（TTS）和/或永久性阈移（PTS）对中枢听觉通路关键结构中神经元细胞密度的影响。在麻醉下，将小鼠暴露于 115dB 声压级（SPL）的噪声中（3 小时，5-20kHz），并在暴露后立即（TTS 组，n=5）或 1 周后（PTS 组，n=6）进行调查。未暴露的动物作为对照（n=7）。记录频率特异性听脑干反应（ABR）以检查听觉阈值。在背（DCN）和腹（VCN）耳蜗核；下丘中央核（ICC）；内侧膝状体的背、腹和内侧亚区（MGBd、MGBv 和 MGBm）；以及初级听觉皮层（AI I-VI）的 I-VI 层中确定细胞密度。与对照组相比，TTS 组（52-69dB SPL）和 PTS 组（33-42dB SPL）的 ABR 阈值显着升高。仅在 TTS 组的 VCN 中观察到细胞密度显着降低（-10%），这很可能是由于神经元的急性过度刺激所致。除了 AI 的 II 层（VCN：-30%和 DCN：-30%（高频）；-39%（低频）；ICC：-31%；MGBd：-31%；MGBm：-28%；MGBv：-31%；AI：-10 至 14%）外，在所有研究的听觉结构中，在暴露后 1 周（PTS 组）时，细胞密度均显着降低。因此，单次噪声暴露后，中枢听觉通路的神经元细胞结构发生了剧烈变化。本研究结果有助于临床医生更好地理解 NIHL 的复杂心理声学现象。
