Socioemotional Behavior and Amygdala-Based Circuitry in Primates
Socioemotional Behavior and Amygdala-Based Circuitry in Primates
批准号:
8255568
负责人:
Ludise Malkova
金额:
$37.99万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2008
资助国家:
美国
项目状态:
已结题
起止时间:
2008-08-19 至 2014-04-30
关键词:
AccountingAcuteAdolescentAggressive behaviorAgonistAmygdaloid structureAnimal ModelAnti-Anxiety AgentsAnxietyAnxiety DisordersAttenuatedAutistic DisorderBehaviorBehavioralBicucullineBrainCell NucleusDiagnosticDiazepamDisinhibitionDoseEmotionalEtiologyEvaluationFrightGABA AgonistsGABA AntagonistsGroomingHumanImpairmentImpulsivityIndividualInfusion proceduresLesionMediatingMental DepressionMidbrain structureMonkeysMood DisordersMuscimolNetwork-basedNeurobiologyNon-Rodent ModelOutcomeOutputPathologyPatientsPatternPlayPrimatesProcessPsychopathologyReceptor ActivationRegulationResearchRewardsRodentRoleSex CharacteristicsSiteSocial BehaviorSocial InteractionSocial PhobiaSpecificityStimulusSystemTectum MesencephaliTestingTherapeuticTherapeutic InterventionWithdrawalWorkaffiliative behaviorbasebicuculline methiodideemotional reactionemotional stimulusgamma-Aminobutyric Acidinterestneuropsychiatrynonhuman primatenovelpreventreceptorrelating to nervous systemresponsesexsocialsuperior colliculus Corpora quadrigemina
中文摘要
描述(由申请人提供):该提案旨在确定大脑中负责异常社会情绪行为的神经基质。这种理解对于开发诊断和治疗方法来识别和治疗情感和焦虑症等神经精神疾病中的异常脑回路至关重要。社会行为研究领域仍然缺乏适当的动物模型,用于社会病理学,导致不适当的攻击,社交焦虑/恐惧,社交退缩/分离,冲动或防御。在非啮齿动物模型中研究社会行为的神经生物学特别有前途,因为社会互动和情感处理的损伤产生了类似于在人类患者中观察到的精神病理学的精神病学。此外,这些研究将允许在啮齿动物中不可行的水平上分析社会互动。因此,这项工作有望大大推进我们对人类社会互动的规范和病理学神经基质的理解,特别是与焦虑和抑郁症的相关性。拟议的研究旨在调查杏仁核为基础的网络,调节社会情绪反应,以占不平衡,可以引起精神病理学在没有结构性病变的新组件。将分析DLSC操作对杏仁核内去抑制诱发的行为异常的脆弱性的影响,以确定DLSC在介导和/或调节杏仁核电路的影响中的作用。 对杏仁核衍生和丘衍生的防御性和攻击性情绪调节之间的功能关系的理解有望揭示情感和焦虑障碍的病因学和治疗干预的新靶点。
英文摘要
DESCRIPTION (provided by applicant): The proposal aims to identify the neural substrates in the brain that are responsible for abnormal socio-emotional behavior. This understanding is vital for developing both diagnostic and therapeutic approaches to identify and treat the abnormal brain circuitry in neuropsychiatric conditions such as affective and anxiety disorders. The field of social behavior research still lacks appropriate animal models for social pathology that leads to inappropriate aggression, social anxiety/phobias, social withdrawal/detachment, impulsivity, or defensiveness. The study of the neurobiology of social behavior in non-rodent models is especially promising since the impairment in social interactions and emotional processing generates symptomatology that resembles psychopathology observed in human patients. Moreover these studies will permit an analysis of social interactions at a level not feasible in rodents. Therefore, this work promises to substantially advance our understanding of the neural substrates of human social interactions in the norm and pathology with a special relevance to anxiety and depression. The proposed research seeks to investigate the novel components of the amygdala-based network that regulates socioemotional responses in order to account for imbalances that can give rise to psychopathology in the absence of structural lesions. The effects of the DLSC manipulations on the vulnerability to behavioral abnormalities evoked by disinhibition within nuclei of the amygdala will be analyzed to determine the role of DLSC in mediating and/or modulating the influence of the amygdala circuitry. An understanding of the functional relationship between the amygdala-derived and colliculus- derived regulation of defensive and aggressive emotional tone is expected to reveal novel targets for both etiology and therapeutic intervention for affective and anxiety disorders.
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会议论文
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