AUDITORY EXPERIENCE AND ADULT NEURON TURNOVER IN BIRDS

描述：（改编自申请人摘要） 在包括人类在内的许多脊椎动物中，神经发生持续到成年期。一个 了解控制神经元增加和存活的因素可能 最终导致对成人神经发生功能的了解，并建议 大脑修复的机制在成年温血脊椎动物中， 神经元的广泛产生发生在鸟类端脑中。在 在鸣禽中，许多新的神经元被插入到高音中心（HVC）， 区域必要的感知和生产的学习发声。 新的HVC神经元取代已经死亡的旧神经元。最近的研究表明， 听觉输入对于正常的神经元替换率是必要的。可用 数据表明，震耳欲聋减少了HVC神经元的数量， 并使其随后的生存。建议的工作将直接测试 成功整合到神经元中的神经元的寿命 HVC在震耳欲聋之前是增强的。进一步的研究将确定是否 震耳欲聋的声音会影响成年神经元的产生或早期存活。 一项病变研究将测试是否外侧大细胞核的 前新纹状体（lMAN），一个必要的区域的歌曲学习，参与 HVC神经元转换的听觉控制。 同种歌曲的播放增加了HVC神经元的活动率 并且通过播放鸟自己的歌声获得最大速率。因此 耳聋对HVC神经元周转的影响可能是由于剥夺了鸟类的 与歌曲相关的听觉刺激拟议的实验将系统地 剥夺听力完好的鸟类获得自我产生的听觉反馈的机会 和/或同种的歌曲来测试这个假设。我们将对比这些影响 通过以下操作，在不完全阻断的情况下， 来自歌唱的自发听觉反馈。这些研究将 探索控制成年神经元增加的感觉要求， 在一个离散的，特征良好的神经系统控制一个学习的损失 发声行为

DESCRIPTION: (adapted from applicant's abstract) Neurogenesis persists into adulthood in many vertebrates including humans. An understanding of the factors that control neuron addition and survival may ultimately lead to insights on the functions of adult neurogenesis and suggest mechanisms for brain repair. In adult warm-blooded vertebrates, the most widespread production of neurons occurs in the avian telencephalon. In songbirds, many new neurons are inserted into the High Vocal Center (HVC), a region necessary for the perception and production of learned vocalizations. New HVC neurons replace older neurons that have died. Recent work shows that auditory input is necessary for normal rates of neuronal replacement. Available data suggest that deafening decreases the numbers of HVC neurons incorporated and prolongs their subsequent survival. Proposed work will directly test whether the life span of neurons that have been successfully incorporated into HVC prior to deafening is augmented. Additional studies will determine whether deafening influences the production or early survival of adult-formed neurons. A lesion study will test whether the lateral magnocellular nucleus of the anterior neostriatum (lMAN), an area necessary for song learning, participates in the auditory control of HVC neuron turnover. Playbacks of conspecific song produce increased rates of HVC neuron activity and maximal rates are obtained with playbacks of the bird's own song. Thus, the effects of deafening on HVC neuronal turnover may be due to depriving birds of song-related auditory stimulation. Proposed experiments will systematically deprive hearing-intact birds of access to self-generated auditory feedback and/or conspecific song to test this hypothesis. We will contrast these effects with those following manipulations that alter, without completely blocking, self-generated auditory feedback from singing. Collectively, these studies will explore the sensory requirements for the control of adult neuron addition and loss within a discrete, well-characterized neural system controlling a learned vocal behavior.