Repeated exposure to stress has been implicated in inducing chronic anxiety states. Stress related increases in anxiety responses are likely mediated by activation of corticotropin-releasing factor receptors (CRFR) in the amygdala, particularly the basolateral amygdala (BLA). Within the BLA, acute injections of the CRFR agonist urocortin 1 (Ucn1) leads to acute anxiety, whereas repeated daily injections of subthreshold-doses of Ucn1 produces a long-lasting, persistent anxiety-like phenotype, a phenomenon referred to as Ucn1-priming. Relative gene expressions from the BLA of vehicle and Ucn1-primed rats were analyzed with quantitative RT-PCR using a predesigned panel of 82 neuroscience-related genes. Compared to vehicle-primed rats, only expression of the somatostatin receptor 2 gene (Sstr2) was significantly reduced in the BLA of Ucn1-primed rats. The contribution of Sstr2 on an anxiety phenotype was tested by injecting a Sstr2 antagonist into the BLA in un-primed rats. The Sstr2 antagonist increased anxiety-like behavior. Notably, pretreatment with Sstr2 agonist injected into the BLA blocked anxiety-inducing effects of acute Ucn1 BLA-injections and delayed anxiety expression during Ucn1-priming. However, concomitant Sstr2 agonist pretreatment during Ucn-1 priming did not prevent either the development of a chronic anxiety state or a reduction of BLA Sstr2 expression induced by priming. The data demonstrate that the persistent anxiety-like phenotype observed with Ucn1-priming in the BLA is associated with a selective reduction of Sstr2 gene expression. Although Sstr2 activation in the BLA blocks acute anxiogenic effects of stress and down-regulation of BLA Sstr2, it does not suppress the long-term consequences of prolonged exposure to stress-related challenges.

反复暴露于压力与诱发慢性焦虑状态有关。与压力相关的焦虑反应增加可能是由杏仁核中促肾上腺皮质激素释放因子受体 (CRFR) 的激活介导的，尤其是基底外侧杏仁核 (BLA)。在 BLA 中，急性注射 CRFR 激动剂尿皮质素 1 (Ucn1) 会导致急性焦虑，而每天重复注射低于阈值剂量的 Ucn1 会产生持久、持续的焦虑样表型，这种现象称为 Ucn1 启动. 使用预先设计的 82 个神经科学相关基因组，通过定量 RT-PCR 分析了载体和 Ucn1 引发大鼠的 BLA 的相关基因表达。与载体引发的大鼠相比，Ucn1 引发的大鼠的 BLA 中只有生长抑素受体 2 基因 (Sstr2) 的表达显着降低。通过将 Sstr2 拮抗剂注射到未致敏大鼠的 BLA 中，测试了 Sstr2 对焦虑表型的贡献。Sstr2 拮抗剂增加了类似焦虑的行为。值得注意的是，用注射到 BLA 中的 Sstr2 激动剂进行预处理可阻断急性 Ucn1 BLA 注射的焦虑诱导作用，并延迟 Ucn1 启动期间的焦虑表达。然而，在 Ucn-1 启动期间伴随的 Sstr2 激动剂预处理并不能阻止慢性焦虑状态的发展或启动诱导的 BLA Sstr2 表达的减少。数据表明，在 BLA 中使用 Ucn1 启动观察到的持续性焦虑样表型与 Sstr2 基因表达的选择性减少有关。尽管 BLA 中的 Sstr2 激活阻止了应激的急性焦虑效应和 BLA Sstr2 的下调，