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.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此，可以在其他清晰的条目中表示。列出的机构是 对于中心，这不一定是调查员的机构。 在报告期间，我们发现Cannibinoid受体1拮抗剂阻断条件恐惧的灭绝，并且可以通过胆囊基蛋白受体拮抗剂逆转。 这表明内源性大麻素通常会抑制胆囊动蛋白的释放，这会破坏恐惧灭绝。 我们发现可卡因增加了恒河猴中的声学惊吓反射，这种作用在慢性可卡因给药后的耐受性并没有减缓。 嗅觉恐惧调节导致鼻上皮的嗅觉感觉神经元数量增加，因此将嗅觉感觉轴突增加到嗅球中。 此外，我们发现杏仁核中的神经肽y可以促进恐惧灭绝。