Abstract

The basolateral amygdala (BLA) and hippocampus are part of the limbic fear–anxiety circuit and have also been implicated in the stress response. The BLA is rich in the expression of α₁-adrenoceptors. We hypothesized that α₁-adrenoceptors in BLA, may modulate stress-induced anxiety-like behavioral responses and hippocampal CA1 pyramidal neuron spine density. α₁-Adrenoceptors agonist, phenylephrine, or antagonist, prazosin, were microinjected bilaterally into BLA of male Wistar rats 5 minutes before foot-shock stress. Then, anxiety-like behavioral responses to stress were measured on the Open Field Test (OFT) and on the Elevated Plus-maze (EPM). Also, Golgi-Cox staining was used to investigate the hippocampal CA1 pyramidal neuron spine density. The results showed that four consecutive day stress reduced the open arm time, and open arm entry in the EPM. Intra-BLA injection of prazosin reversed stress-induced anxiogenic-like behaviors. In the OFT stress decreased the center area entries and time, while intra-BLA injection of phenylephrine or prazosin did not alter these parameters. Stress also reduced the dendritic and axonal arborization in hippocampal CA1 pyramidal neurons. Interestingly, intra-BLA infusion of prazosin blocked the reduction in dendritic and axonal arborization induced by foot-shock stress. Taken together, stress produces anxiogenic-like behaviors and hippocampal CA1 pyramidal neurons morphology changes, which may be mediated through the BLA α₁-adrenoceptors mechanism.

中文翻译：

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基底外侧杏仁核α1-肾上腺素能受体抑制可减轻应激诱导的海马CA1锥体神经元的焦虑行为和脊柱形态学损害。

摘要

基底外侧杏仁核（BLA）和海马是边缘恐惧-焦虑回路的一部分，也与压力反应有关。该BLA富含的α表达₁肾上腺素能受体。我们假设α ₁ -肾上腺素受体在BLA，可以调节紧张诱发的焦虑样的行为反应和海马CA1区锥体神经元棘密度。α ₁-在足部电击前5分钟，将双肾上腺素受体激动剂去氧肾上腺素或拮抗剂吡唑嗪双侧注射到雄性Wistar大鼠的BLA中。然后，在旷场测试（OFT）和高架迷宫（EPM）上测量了对压力的焦虑样行为反应。此外，高尔基-科克斯染色用于研究海马CA1锥体神经元的脊柱密度。结果表明，连续四天的压力减少了EPM中的张开时间和张开臂进入时间。BLA内注射哌唑嗪逆转了应激诱导的类似焦虑的行为。在OFT中，应力减少了中心区域的进入和时间，而在BLA内注射去氧肾上腺素或哌唑嗪并没有改变这些参数。压力还减少了海马CA1锥体神经元的树突状和轴突乔化。有趣的是 在BLA内注入哌唑嗪可阻止脚电击引起的树突状和轴突乔化作用的减少。综上所述，压力会产生类似焦虑的行为，海马CA1锥体神经元的形态变化可能是通过BLAα介导的。_1-肾上腺素受体机制。