Auditory cortical tuning to communication sounds and genetic constraints on the vocal learning landscape
听觉皮层对交流声音的调节和声乐学习环境的遗传限制
基本信息
- 批准号:10607688
- 负责人:
- 金额:$ 4.68万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2022
- 资助国家:美国
- 起止时间:2022-09-01 至 2025-08-31
- 项目状态:未结题
- 来源:
- 关键词:AcousticsAdolescentAdultAffectAnimal ModelAnimalsAuditoryAuditory Perceptual DisordersAuditory areaBehaviorBehavioralBehavioral GeneticsBirdsCarrying CapacitiesCharacteristicsChildCodeCommunicationDataData AnalysesDevelopmentDiseaseElectrophysiology (science)FathersFosteringFoundationsGene MutationGenesGeneticGenetic IdentityGoalsGrantHearingHearing problemHeritabilityHomeHumanHybridsImpairmentInfantInstitutesInvestigationJournalsLanguageLeadLearningLifeLife ExperienceMeasuresMorphologyNeuronsOutcomeParentsPatternPerceptionProcessProductionPublicationsResearchSensoryShapesShort-Term MemorySingle ParentSocial InteractionSongbirdsSourceSpeechSpeech SoundStimulusStructureSupport SystemTestingTimeTrainingTwin StudiesUniversitiesVoiceWorkWritingautism spectrum disorderawakebasecareercode developmentcommunication behaviordevelopmental diseaseexperienceexperimental studygenetic makeupgenome-wideinsightlanguage processinglearning abilitylong term memoryneuroimagingpreventreceptive fieldrelating to nervous systemresponsesensory mechanismsensory systemskillssocialsoundspecific language impairmentspeech processingsymposiumsyntaxtutoringvocal learningvocalization
项目摘要
Project Summary
Hearing and speech are fundamental to human communication. Before infants are 12 months old, they
have learned the statistical regularities of speech sounds around them, which guides vocal learning throughout
early life and permanently alters auditory coding in cortical neurons. Deficits in cortical speech coding are
hallmarks of central auditory disorders such as auditory processing disorder (APD), specific language
impairment (SLI), and autism spectrum disorder (ASD), which together affect an estimated 7% of children.
These disorders are highly heritable and involve additive effects of multiple gene mutations. But, how genes
constrain the landscape through which auditory coding unfolds over development is entirely unknown. The
proposed aims test specific hypotheses regarding genetic constraints on auditory coding in songbirds, an
animal model of speech processing. Like humans and unlike other animals, songbirds learn to sing by learning
regularities in the vocal sounds of adults they interact with socially, and auditory cortical coding is permanently
altered by experience. The songbird secondary auditory cortex, caudomedial nidopallium (NCM) is required for
vocal learning, and contains neurons that are selectively tuned for acoustics of songs heard in early life.
Preliminary behavioral data indicate that juveniles raised by birds of a different species learn the morphologic
structure of their foster father’s song, but arrange their song with temporal structure typical of their genetic
relatives, despite never having heard those songs. In contrast, hybrid birds born of mixed-species parents copy
both the morphology and temporal structure of their father’s song, despite having only half the genetic makeup.
These data lead me to hypothesize that separate subpopulations of NCM neurons selectively code for
song morphology and temporal structure (Aim 1), and that temporal coding is constrained by genetics
(Aim 2). I propose to analyze singing behavior in songbirds with differing genetic backgrounds and specific
differences in singing behavior. I will compare electrophysiological responses of their NCM neurons to natural
songs, songs with altered temporal structure, and synthetic sounds that systematically vary in acoustics and
timing. I will use neural encoding analyses to measure which stimulus features drive responses, and decoding
analyses to measure what information neurons carry about stimuli. Expected outcomes will provide
fundamental insights into the genetic sources of limitations on cortical auditory coding capacity, and will inform
mechanism-based approaches to treating central auditory disorders such as APD, SLI, and ASD. The training
plan includes training in electrophysiology in awake animals, advanced neural data analyses, developing
expertise in behavioral genetics, and writing for journal publications, grants, and conference presentations.
Training will take place in the sponsor’s and co-sponsor’s labs, housed in Columbia University’s Zuckerman
Institute. The Institute is home to world-renowned neuroscientists and state-of-the-art facilities.
项目摘要
听觉和言语是人类交流的基础。在婴儿12个月大之前,他们
我学习了他们周围语音的统计规律,这在整个声乐学习中都是有指导作用的
并永久性地改变了大脑皮层神经元的听觉编码。皮质语音编码的缺陷有
中枢性听觉障碍的特征,如听觉处理障碍(APD)、特定语言
损害(SLI)和自闭症谱系障碍(ASD),估计有7%的儿童受到影响。
这些疾病具有高度的遗传性,涉及多个基因突变的相加效应。但是,基因是如何
限制听觉编码在开发过程中展开的场景是完全未知的。这个
拟议的目标测试了关于鸣禽听觉编码的遗传限制的特定假设,以及
语音处理的动物模型。像人类一样,不同于其他动物,鸣禽通过学习来学习唱歌
与他们进行社交互动的成年人的声音有规律,听觉皮质编码是永久性的
被经验改变了。鸣禽的次级听觉皮质,尾内侧nidopallium(NCM)是
声乐学习,包含有选择性地调谐的神经元,用于在生命早期听到的歌曲的声学。
初步的行为数据表明,由不同物种的鸟类饲养的幼鸟学习形态
他们养父歌曲的结构,但用典型的遗传时间结构来安排他们的歌曲
亲戚,尽管从来没有听过这些歌。相比之下,混合物种父母所生的杂交鸟类会复制
他们父亲歌曲的形态和时间结构,尽管只有一半的基因构成。
这些数据让我假设,不同的NCM神经元亚群选择性地编码
歌曲形态和时间结构(目标1),时间编码受遗传学限制
(目标2)。我建议分析具有不同遗传背景和特定基因的鸣鸟的鸣叫行为
歌唱行为的差异。我会将他们的NCM神经元的电生理反应与自然的
歌曲,具有改变的时间结构的歌曲,以及声学和系统地改变的合成声音
时机到了。我将使用神经编码分析来衡量哪些刺激特征驱动反应,以及解码
分析以测量神经元携带的关于刺激的信息。预期结果将提供
对皮质听觉编码能力受限的遗传来源的基本见解,并将提供信息
以机制为基础的治疗中枢性听觉障碍的方法,如雪崩、系统性红斑狼疮和自闭症。培训
计划包括清醒动物的电生理学培训,高级神经数据分析,开发
行为遗传学方面的专业知识,以及为期刊出版物、赠款和会议演示文稿撰写文章。
培训将在赞助商和联合赞助商的实验室进行,实验室设在哥伦比亚大学的扎克曼
研究所。该研究所聚集了世界知名的神经科学家和最先进的设施。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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