LMAN lesions prevent song degradation after deafening without reducing HVC neuron addition.
LMAN lesions prevent song degradation after deafening without reducing HVC neuron addition.
复制标题
LMAN 损伤可防止震耳欲聋后歌曲退化，而不减少 HVC 神经元的添加。
DOI：
10.1002/dneu.20508
复制
发表时间：
2007
影响因子：
3
通讯作者：
Nordeen,KathyW
中科院分区：
文献类型：
--
作者：
Scott,LuisaL;Nordeen,ErnestJ;Nordeen,KathyW
In some songbirds perturbing auditory feedback can promote changes in song structure well beyond the end of song learning. One factor that may drive vocal change in such deafened birds is the ongoing addition of new vocal‐motor neurons into the song system. Without auditory feedback to guide their incorporation, the addition of these new neurons could disrupt the established song pattern. To assess this hypothesis, the authors determined if neuronal recruitment into the vocal motor nucleus HVC is affected by neural signals that influence vocal change in adult deafened birds. Such signals appear to be conveyed via LMAN, a nucleus in the anterior forebrain that is necessary for vocal change after deafening. Here the authors tested whether LMAN lesions might restrict song degradation after deafening by reducing the addition or survival of new HVC neurons that would otherwise corrupt the ongoing song pattern. Using [3H]thymidine autoradiography to identify neurons generated in adult zebra finches, it was shown here that LMAN lesions do not reduce the number or percent of new HVC neurons surviving for either several weeks or months after [3H]thymidine labeling. However, the authors confirmed previous reports that LMAN lesions restrict vocal change after deafening. These data suggest that neurons incorporated into the adult HVC may form behaviorally adaptive connections without requiring auditory feedback, and that any role such neurons may play in promoting vocal change after adult deafening requires anterior forebrain pathway output. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007.
