Puel J L, Ruel J, Gervais d'Aldin C, Pujol R
INSERM-U.254 et Université Montpellier I, Laboratoire de Neurobiologie de l'Audition, CHU Hôpital St. Charles, France.
Neuroreport. 1998 Jun 22;9(9):2109-14. doi: 10.1097/00001756-199806220-00037.
Guinea-pigs were exposed to a traumatic sound inducing up to 80 dB hearing loss. Beside the well described mechanical damage to outer hair cells, a total disruption of inner hair cell (IHC)-auditory nerve synapses was acutely observed within the traumatized area. To test the hypothesis that synaptic damage is due to an excessive release of glutamate by the IHCs, we examined the protective effect of the glutamate antagonist kynurenate on noise-induced hearing loss. The high degree of protection observed with kynurenate attests that dendritic damage is an important component in noise-induced hearing loss. Moreover, we demonstrate that a synaptic repair mechanism occurring within the first few days post-exposure is partly responsible for the recovery of temporary threshold shifts after an acoustic trauma.
将豚鼠暴露于可导致高达80分贝听力损失的创伤性声音中。除了已被充分描述的外毛细胞机械损伤外,在受创伤区域内还急性观察到内毛细胞(IHC)-听觉神经突触的完全破坏。为了验证突触损伤是由于IHC过量释放谷氨酸所致这一假设,我们研究了谷氨酸拮抗剂犬尿喹啉酸对噪声性听力损失的保护作用。犬尿喹啉酸所观察到的高度保护作用证明树突损伤是噪声性听力损失的一个重要组成部分。此外,我们证明暴露后最初几天内发生的突触修复机制部分负责了声创伤后暂时阈移的恢复。