Acute stress causes rapid synaptic insertion of Ca2+ -permeable AMPA receptors to facilitate long-term potentiation in the hippocampus.
Acute stress causes rapid synaptic insertion of Ca2+ -permeable AMPA receptors to facilitate long-term potentiation in the hippocampus.
复制标题
急性应激会导致CA2+可渗透AMPA受体的快速突触插入，以促进海马的长期增强。
DOI：
10.1093/brain/awt293
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发表时间：
2013-12
期刊：
影响因子：
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通讯作者：
Cho K
中科院分区：
文献类型：
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作者：
Whitehead G;Jo J;Hogg EL;Piers T;Kim DH;Seaton G;Seok H;Bru-Mercier G;Son GH;Regan P;Hildebrandt L;Waite E;Kim BC;Kerrigan TL;Kim K;Whitcomb DJ;Collingridge GL;Lightman SL;Cho K
神经内分泌对急性应激的反应对于生存至关重要，而对慢性应激的长期反应可能是有害的。学习和记忆特别容易受到压力的影响，认知缺陷是慢性压力的明显后果。尽管有充分的证据表明急性压力可以增强认知能力，但其机制尚不清楚。我们发现，无论是在 30 分钟约束应激后从大鼠身上制备的海马切片，还是直接暴露于糖皮质激素的海马切片，都表现出不依赖于 N-甲基-d-天冬氨酸受体的长期增强形式。我们证明该机制涉及 NMDA 受体和 PKA 依赖性 Ca2+ 渗透性 AMPA 受体插入突触。然后，这些在高频刺激期间触发额外的 NMDA 受体独立形式的 LTP。
The neuroendocrine response to episodes of acute stress is crucial for survival whereas the prolonged response to chronic stress can be detrimental. Learning and memory are particularly susceptible to stress with cognitive deficits being well characterized consequences of chronic stress. Although there is good evidence that acute stress can enhance cognitive performance, the mechanism(s) for this are unclear. We find that hippocampal slices, either prepared from rats following 30 min restraint stress or directly exposed to glucocorticoids, exhibit an N-methyl-d-aspartic acid receptor-independent form of long-term potentiation. We demonstrate that the mechanism involves an NMDA receptor and PKA-dependent insertion of Ca2+-permeable AMPA receptors into synapses. These then trigger the additional NMDA receptor-independent form of LTP during high frequency stimulation.