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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Tissue plasminogen activator promotes the effects of corticotropin-releasing factor on the amygdala and anxiety-like behavior.
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Tissue plasminogen activator promotes the effects of corticotropin-releasing factor on the amygdala and anxiety-like behavior.

机译：组织纤溶酶原激活剂促进促肾上腺皮质激素释放因子对杏仁核和焦虑样行为的影响。

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摘要

Stress-induced plasticity in the brain requires a precisely orchestrated sequence of cellular events involving novel as well as well known mediators. We have previously demonstrated that tissue plasminogen activator (tPA) in the amygdala promotes stress-induced synaptic plasticity and anxiety-like behavior. Here, we show that tPA activity in the amygdala is up-regulated by a major stress neuromodulator, corticotropin-releasing factor (CRF), acting on CRF type-1 receptors. Compared with WT, tPA-deficient mice responded to CRF treatment with attenuated expression of c-fos (an indicator of neuronal activation) in the central and medial amygdala but had normal c-fos responses in paraventricular nuclei. They exhibited reduced anxiety-like behavior to CRF but had a sustained corticosterone response after CRF administration. This effect of tPA deficiency was not mediated by plasminogen, because plasminogen-deficient mice demonstrated normal behavioral and hormonal changes to CRF. These studies establish tPA as an important mediator of cellular, behavioral, and hormonal responses to CRF.
机译：压力诱导的大脑可塑性需要精确地精心安排的一系列细胞事件，涉及新颖的和众所周知的介质。我们以前已经证明杏仁核中的组织纤溶酶原激活剂（tPA）促进应激诱导的突触可塑性和焦虑样行为。在这里，我们显示杏仁核中的tPA活性是由作用于CRF 1型受体的主要应激神经调节剂促肾上腺皮质激素释放因子（CRF）上调的。与野生型相比，tPA缺陷型小鼠对杏仁核中央和内侧杏仁核的c-fos表达减弱（对神经元激活的指示），但对CRF治疗有反应，但在室旁核中的c-fos反应正常。他们对CRF表现出减少的焦虑样行为，但在CRF给药后具有持续的皮质酮反应。 tPA缺乏的这种影响不是由纤溶酶原介导的，因为纤溶酶原缺陷的小鼠表现出CRF的正常行为和激素变化。这些研究将tPA确立为对CRF的细胞，行为和激素反应的重要介体。

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