COLLABORATIVE MOOD DISORDERS INITIATIVE

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目及 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 本研究的目的是评估促肾上腺皮质激素释放因子1受体（CRF 1）拮抗剂在我们的恐惧和焦虑大鼠的措施，并比较它与我们的条件性恐惧的措施的影响。我们发现，GSK CRF 1拮抗剂块声惊吓幅度的增加时，大鼠给予CRF室内或当他们暴露在强光下很长一段时间，但不是当惊吓增加的存在下，先前配对的提示与足电击。 由于前两个焦虑指标依赖于大脑中一个叫做终纹床核的区域，而最后一个指标依赖于杏仁核，我们认为CRF拮抗剂可能通过阻断终纹床核中的受体起作用。我们发现，使用病毒载体基因转移在杏仁核中央核中CRF的过度表达导致了几项指标的持续增加，这表明焦虑的持续增加。

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. The objective of this study is to evaluate the effects of corticotropin releasing factor 1 receptor (CRF 1) antagonists in our measures of fear and anxiety in rats and compare it to our measure of conditioned fear. We found that the GSK CRF 1 antagonist blocks the increase in acoustic startle amplitude when rats are given CRF intraventricular or when they are exposed to bright light for long periods of time but not when startle is increased in the presence of a cue previously paired with footshock. Because the first two measures of anxiety are dependent on a brain area called the bed nucleus of the stria terminalis, but the last measure is dependent on the amygdala, we believe that the CRF antagonist may work by blocking receptors in the bed nucleus of the stria terminalis. We found that over-expression of CRF in the central nucleus of the amygdala using viral vector gene transfer leads to a persistent increase in several measures that suggests a persistent increase in anxiety.