Sensory- and motor-driven genes in vocal communication

描述（由申请人提供）：本提案的目标是识别正常和痴呆受试者中通过学习语音交流激活的感觉和运动驱动基因。我们将使用的动物模型是鸣禽。鸣禽是唯一一种可以研究人类语言基础的非人类动物。非人类的灵长类动物、啮齿类动物和其他通常被研究的动物没有这种能力。在鸣禽中，听到特定物种的发声（感觉活动）会诱导整个听觉通路的基因表达大幅增加。这种感觉驱动的表达是经验依赖的，因为诱导要求鸟类与成年同种动物一起饲养，当鸟类听到新的物种特异性歌曲时，诱导最高。表情被震耳欲聋挡住了。产生模仿发声的行为（运动活动）诱导整个大脑发声通路的基因表达大幅增加，并且这种运动驱动的表达不会被震耳欲聋所阻断。然而，当鸟类像人类一样被激怒时，它们习得的发声能力就会恶化。这种退化，在鸣禽中，是一个主动的过程，需要基底神经节皮质样的发声通路，其中发声驱动的基因expression. To日期，很少有基因已被确定与这种感觉和运动驱动的调节行为过程中，尚未被确定的变化，与麻醉诱导的退化学习发声。据信，整个基因调控网络在这些行为过程中被激活。我们将使用行为，神经解剖学，和高通量分子生物学方法来识别和表征感官和电机驱动的基因激活正常的声乐交流和学习发声的退化引起的。由于大多数鸣禽基因有显着的同源性，已知的哺乳动物基因，我们的实验将使我们能够确定鸟类的大脑基因与人类/哺乳动物的同源性服从实验表征鸣禽系统。

DESCRIPTION (provided by applicant): The goal of this proposal is to identify sensory- and motor-driven genes activated by learned vocal communication in normal and deafened subjects. The animal model we will utilize is a songbird. Songbirds are one of the only accessible non-human animals where learned vocal communication, the substrate for human language, can be studied. Non-human primates, rodents, and other commonly studied animals do not have; this ability. In songbirds, hearing species-specific vocalizations (sensory activity) induces large increases of gene expression throughout the auditory pathway. This sensory-driven expression is experience-dependent, as induction requires that the birds be raised with adult conspecifics and induction is highest when the birds hear novel species-specific songs. The expression is blocked by deafening. The act of producing imitated vocalizations (motor activity) induces large increases of gene expression throughout the cerebral vocal pathway, and this motor-driven expression is not blocked by deafening. However, when birds are deafened, like humans, their learned vocalizations deteriorate. This deterioration, in songbirds, is an active process that requires the basal ganglia cortical-like vocal pathway, in which vocalizing-driven gene expression is found. To date, few genes have been identified with such sensory- and motor-driven regulation during behavior and none have yet been identified that change with deafening-induced deterioration of learned vocalizations. It is believed that an entire gene regulatory network is activated in these behavioral processes. We will use behavioral, neuroanatomical, and high throughput molecular biological approaches to identify and characterize sensory and motor-driven genes activated by normal vocal communication and by deafened-induced deterioration of learned vocalizations. Since most songbird genes have significant homology to known mammalian genes our experiments will enable us to identify avian brain genes with humain/mammalian homologues amenable to experimental characterization in the songbird system.