ANATOMY AND PHARMACOLOGY OF FEAR-POTENTIATED STARTLE

恐惧增强惊吓的解剖学和药理学

• 批准号: 8172349
• 负责人: MICHAEL NMN DAVIS
• 金额: $ 4.39万
• 依托单位: EMORY UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-05-01 至 2011-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8172349
• 关键词: Acoustics; Afferent Neurons; Amygdaloid structure; Anatomy; Axon; Cholecystokinin; Cholecystokinin Receptor; Chronic; Cocaine; Computer Retrieval of Information on Scientific Projects Database; Endocannabinoids; Extinction (Psychology); Fright; Funding; Grant; Institution; Macaca mulatta; Nasal Epithelium; Pharmacology; Reflex action; Reporting; Research; Research Personnel; Resources; Sensory; Source; United States National Institutes of Health; conditioned fear; neuropeptide Y; olfactory bulb; receptor

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. During the reporting period, we found that the cannibinoid receptor 1 antagonist blocks extinction of conditioned fear and that this can be reversed by a cholecystokinin receptor antagonist. This suggested that endocannabinoids normally inhibit release of cholecystokinin which can disrupt fear extinction. We found that cocaine increased the acoustic startle reflex in rhesus monkeys and that this effect did not slow tolerance after chronic cocaine administration. Olfactory fear conditioning led to an increase in the number of olfactory sensory neurons in the nasal epithelium and therefore increased olfactory sensory axons into the olfactory bulb. Additionally, we found that neuropeptide Y in the amygdala can facilitate fear extinction.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目和 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 在报告期间，我们发现大麻素受体 1 拮抗剂可以阻止条件性恐惧的消失，而胆囊收缩素受体拮抗剂可以逆转这种情况。 这表明内源性大麻素通常会抑制胆囊收缩素的释放，从而破坏恐惧的消退。 我们发现可卡因增加了恒河猴的听觉惊吓反射，并且这种作用并没有减缓长期服用可卡因后的耐受性。 嗅觉恐惧调节导致鼻上皮中嗅觉感觉神经元数量增加，因此进入嗅球的嗅觉感觉轴突增加。 此外，我们发现杏仁核中的神经肽 Y 可以促进恐惧消退。