Bed nuclei of the stria terminalis modulate memory consolidation via glucocorticoid-dependent and -independent circuits.
Bed nuclei of the stria terminalis modulate memory consolidation via glucocorticoid-dependent and -independent circuits.
复制标题
终纹床核通过糖皮质激素依赖性和非依赖性回路调节记忆巩固。
DOI：
10.1073/pnas.1915501117
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发表时间：
2020
影响因子：
11.1
通讯作者：
Radley,JasonJ
中科院分区：
文献类型：
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作者：
Lingg,RyanT;Johnson,ShaneB;Emmons,EricB;Anderson,RachelM;Romig-Martin,SaraA;Narayanan,NandakumarS;McGaugh,JamesL;LaLumiere,RyanT;Radley,JasonJ
有大量证据表明，糖皮质激素能增强记忆，帮助确保重要的情感事件被人们牢记。先前的研究结果表明，终纹床核的前腹侧区域(AvBST)调节糖皮质激素的释放，这表明avBST的活动可能会影响情绪唤醒学习事件后的记忆巩固。为了研究这一问题，雄性SD大鼠接受了抑制性回避训练和重复测量应激激素，然后立即对avBST或其向下游区域的投射进行光遗传操作，并在48小时后测试其保持能力。结果表明，avBST抑制可增加训练后的垂体-肾上腺输出，增强对抑制性回避训练的记忆。用糖皮质激素合成抑制剂预处理可阻断记忆增强和增强的皮质酮反应，表明记忆增强依赖于训练后即刻的糖皮质激素释放。相比之下，训练后的avBST刺激减少了保持能力，但对应激激素输出没有影响。随后的实验表明，抑制avBST对下丘脑室旁核的输入会增加应激激素的输出和随后的保留，而刺激对两者都没有影响。相反，刺激(但不是抑制)avBST传入中脑导水管周围灰质腹外侧区会损害固结，而两种手法都不会影响糖皮质激素的分泌。这些发现表明，avBST的不同通路分别通过糖皮质激素依赖和非依赖机制对avBST抑制和刺激的助记效应起作用。
There is extensive evidence that glucocorticoid hormones enhance memory consolidation, helping to ensure that emotionally significant events are well remembered. Prior findings suggest that the anteroventral region of bed nuclei of the stria terminalis (avBST) regulates glucocorticoid release, suggesting the potential for avBST activity to influence memory consolidation following an emotionally arousing learning event. To investigate this issue, male Sprague-Dawley rats underwent inhibitory avoidance training and repeated measurement of stress hormones, immediately followed by optogenetic manipulations of either the avBST or its projections to downstream regions, and 48 h later were tested for retention. The results indicate that avBST inhibition augmented posttraining pituitary–adrenal output and enhanced the memory for inhibitory avoidance training. Pretreatment with a glucocorticoid synthesis inhibitor blocked the memory enhancement as well as the potentiated corticosterone response, indicating the dependence of the memory enhancement on glucocorticoid release during the immediate posttraining period. In contrast, posttraining avBST stimulation decreased retention yet had no effect on stress hormonal output. Subsequent experiments revealed that inhibition of avBST input to the paraventricular hypothalamus enhanced stress hormonal output and subsequent retention, whereas stimulation did not affect either. Conversely, stimulation—but not inhibition—of avBST input to the ventrolateral periaqueductal gray impaired consolidation, whereas neither manipulation affected glucocorticoid secretion. These findings indicate that divergent pathways from the avBST are responsible for the mnemonic effects of avBST inhibition versus stimulation and do so via glucocorticoid-dependent and -independent mechanisms, respectively.