Corticosterone-induced enhancement of memory and synaptic Arc protein in the medial prefrontal cortex.
Corticosterone-induced enhancement of memory and synaptic Arc protein in the medial prefrontal cortex.
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DOI：
10.1016/j.nlm.2014.02.007
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发表时间：
2014-07
影响因子：
2.7
通讯作者：
McIntyre CK
中科院分区：
文献类型：
--
作者：
McReynolds JR;Holloway-Erickson CM;Parmar TU;McIntyre CK
急性应用应激激素皮质酮可增强记忆巩固，其方式依赖于杏仁核基底外侧复合体(BLA)的调节作用。训练后给予皮质酮可增加海马区突触富集区活性调节细胞骨架相关蛋白(Arc)的表达。干扰海马区Arc的表达会损害记忆，提示皮质酮诱导的海马区Arc的增加在激素增强记忆的作用中起作用。阻断白质中的β受体可减弱皮质酮诱导的海马区Arc表达的增加，并阻断皮质酮诱导的记忆增强。为了确定训练后皮质酮治疗是否影响与记忆处理有关的大脑其他区域突触中Arc蛋白的表达，在抑制性回避训练后立即给大鼠注射增强记忆剂量的皮质酮。在海马区，内侧前额叶皮质(MPFC)的突触部分Arc蛋白表达增加。阻断Arc蛋白的表达显著损害记忆，表明该蛋白在mPFC中是长期记忆形成所必需的。为了验证阻断白质中的β肾上腺素受体将阻断全身皮质酮对记忆的影响并减弱mPFC Arc表达的假设，就像在海马区所做的那样，训练结束后，在全身皮质酮注射的同时，在白质中微量注射β肾上腺素受体拮抗剂心得安。虽然这种治疗阻止了皮质酮诱导的记忆增强，但它增加了皮质酮诱导的mPFC突触部分Arc蛋白的表达。这些发现表明，BLA通过参与皮质酮诱导的传出脑区突触可塑性的负或正调节来介导应激激素对记忆的影响。
Acute administration of the stress hormone corticosterone enhances memory consolidation in a manner that is dependent upon the modulatory effects of the basolateral complex of the amygdala (BLA). Posttraining administration of corticosterone increases expression of the activity-regulated cytoskeletal-associated protein (Arc) in hippocampal synaptic-enriched fractions. Interference with hippocampal Arc expression impairs memory, suggesting that the corticosterone-induced increase in hippocampal Arc plays a role in the memory enhancing effect of the hormone. Blockade of β-adrenoceptors in the BLA attenuates the corticosterone-induced increase in hippocampal Arc expression and blocks corticosterone-induced memory enhancement. To determine whether posttraining corticosterone treatment affects Arc protein expression in synapses of other areas of the brain that are involved in memory processing, a memory-enhancing dose of corticosterone was administered to rats immediately after inhibitory avoidance training. As seen in the hippocampus, Arc protein expression was increased in synaptic fractions taken from the prelimbic region of the medial prefrontal cortex (mPFC). Blockade of Arc protein expression significantly impaired memory, indicating that the protein is necessary in the mPFC for long-term memory formation. To test the hypothesis that blockade of β-adrenoceptors in the BLA would block the effect of systemic corticosterone on memory and attenuate mPFC Arc expression, as it does in the hippocampus, posttraining intra-BLA microinfusions of the β-adrenoceptor antagonist propranolol were given concurrently with the systemic corticosterone injection. Although this treatment blocked corticosterone-induced memory enhancement, it increased corticosterone-induced Arc protein expression in mPFC synaptic fractions. These findings suggest that the BLA mediates stress hormone effects on memory by participating in the negative or positive regulation of corticosterone-induced synaptic plasticity in efferent brain regions.