Harrison R V
Department of Otolaryngology, The Hospital for Sick Children, and University of Toronto, Canada.
Scand Audiol Suppl. 2001(53):8-14. doi: 10.1080/010503901750166529.
Inner hair cell lesions to the basal turn of the cochlea effectively result in a partial deafferentation of the auditory system. At the level of the midbrain (central nucleus of inferior colliculus) cochleotopic maps, based on single unit response characteristic frequency, are changed after such deafferentation. When a cochlear lesion is induced in a neonatal animal (chinchilla), the reorganization of the frequency map is more extensive than that resulting from similar deafferentation in the adult subject. Neonatal cochlear lesions result in an over-representation of sound frequencies corresponding to the border of the cochlear lesion, while similar lesions in the adult do not. The results suggest that significant plasticity exists in the auditory midbrain during early post natal development (even in a precocious species, such as chinchilla); however, this plasticity is largely lost in the mature animal. A conceptual model for the frequency map re-wiring is presented.
耳蜗基部转弯处的内毛细胞损伤会有效导致听觉系统部分传入神经阻滞。在中脑（下丘中央核）水平，基于单单元反应特征频率的耳蜗拓扑图在这种传入神经阻滞后会发生变化。当在新生动物（灰鼠）中诱发耳蜗损伤时，频率图的重组比成年个体类似传入神经阻滞所导致的重组更为广泛。新生动物的耳蜗损伤会导致与耳蜗损伤边界相对应的声音频率过度表征，而成年动物的类似损伤则不会。结果表明，在出生后早期发育过程中（即使在像灰鼠这样早熟的物种中），听觉中脑存在显著的可塑性；然而，这种可塑性在成熟动物中基本丧失。本文提出了一个频率图重新布线的概念模型。
