ANATOMY AND PHARMACOLOGY OF FEAR-POTENTIATED STARTLE

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 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退，这可以被缩胆囊素受体拮抗剂逆转。这表明，内源性大麻素通常会抑制胆囊素的释放，从而扰乱恐惧的消退。 我们发现，可卡因增加了恒河猴的声惊厥反射，这种作用不会减缓长期服用可卡因后的耐受性。嗅觉恐惧条件反射导致鼻上皮中的嗅觉神经元数量增加，从而增加了进入嗅球的嗅觉轴突。 此外，我们发现杏仁核中的神经肽Y可以促进恐惧的消退。

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.