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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Corticotrophin releasing factor-induced synaptic plasticity in the amygdala translates stress into emotional disorders.
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Corticotrophin releasing factor-induced synaptic plasticity in the amygdala translates stress into emotional disorders.

机译：杏仁核中促肾上腺皮质激素释放因子诱导的突触可塑性将压力转化为情绪障碍。

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The amygdala is involved in the associative processes for both appetitive and aversive emotions, and its function is modulated by stress hormones. The neuropeptide corticotrophin releasing factor (CRF) is released during stress and has been linked to many stress-related behavioral, autonomic, and endocrine responses. In the present study, nonanxiety-inducing doses of a potent CRF type 1 and 2 receptor agonist, urocortin (Ucn), was infused locally into the basolateral amygdala (BLA) of rats. After 5 daily injections of Ucn, the animals developed anxiety-like responses in behavioral tests. Intravenous administration of the anxiogenic agent sodium lactate elicited robust increases in blood pressure, respiratory rate, and heart rate. Furthermore, in the absence of any additional Ucn treatment, these behavioral and autonomic responses persisted for >30 d. Whole-cell patch-clamp recordings from BLA neurons of these hyper-reactive animals revealed a pronounced reduction in both spontaneous and stimulation-evoked IPSPs, leading to a hyperexcitability of the BLA network. This Ucn-induced plasticity appears to be dependent on NMDA receptor and subsequent calcium-calmodulin-dependent protein kinase II (CaMKII) activation, because it is blocked by pretreatment with NMDA receptor antagonists and by coadministration of CaMKII inhibitors. Our results show for the first time a stress peptide-induced behavioral syndrome that can be correlated with cellular mechanisms of neural plasticity, a novel mechanism that may explain the etiological role of stress in several chronic psychiatric and medical disorders.
机译：杏仁核参与食性和厌恶性情绪的联想过程，其功能由应激激素调节。神经肽促肾上腺皮质激素释放因子（CRF）在应激过程中被释放，并与许多应激相关的行为，自主和内分泌反应有关。在本研究中，将非焦虑诱导剂量的有效CRF 1型和2型受体激动剂urocortin（Ucn）局部注入大鼠的基底外侧杏仁核（BLA）。每天注射Ucn 5次后，动物在行为测试中出现焦虑样反应。静脉内施用血管生成剂乳酸钠引起血压，呼吸频率和心率的强劲增加。此外，在没有任何其他Ucn治疗的情况下，这些行为和自主反应持续超过30天。这些反应过度的动物的BLA神经元的全细胞膜片钳记录显示自发性IPSP和刺激性IPSP均显着减少，从而导致BLA网络的过度兴奋。这种由Ucn诱导的可塑性似乎取决于NMDA受体和随后的钙钙调蛋白依赖性蛋白激酶II（CaMKII）活化，因为它被NMDA受体拮抗剂预处理和CaMKII抑制剂共同给药所阻断。我们的结果首次显示了应激肽诱导的行为综合症，该综合症可能与神经可塑性的细胞机制有关，这种新机制可以解释应激在几种慢性精神病和医学疾病中的病因作用。

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