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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Bidirectional modulation of hippocampal long-term potentiation under stress and no-stress conditions in basolateral amygdala-lesioned and intact rats.
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Bidirectional modulation of hippocampal long-term potentiation under stress and no-stress conditions in basolateral amygdala-lesioned and intact rats.

机译：基底外侧杏仁核病变和完整大鼠在应激和无应激条件下的海马长时程增强双向调控。

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摘要

Hippocampal long-term potentiation (LTP) is widely considered as a cellular model for learning and memory formation. We have shown previously that protein synthesis-independent, early dentate gyrus (DG) LTP, lasting approximately 4-5 h, can be transformed into a late-LTP with a duration of > or = 24 h by a brief acute swim stress experience (high-stress condition). This reinforcement requires the activation of mineralocorticoid receptors and protein synthesis. The basolateral amygdala (BLA) is known to modulate glucocorticoid effects on the consolidation of spatial/contextual memory via a beta-adrenergic mechanism. Interestingly, hippocampal DG-LTP can also be indirectly modulated by beta-adrenergic and cholinergic/muscarinergic processes. Here, we show that the reinforcement of early-DG-LTP under high-stress conditions depends on the processing of novel spatial/contextual information. Furthermore, this reinforcement was blocked in BLA-lesioned animals compared with sham-operated and intact controls; however, it was not dependent on beta-adrenergic or cholinergic/muscarinergic receptor activation. In contrast, under low-stress conditions, the induction of late-LTP in BLA-lesioned animals is facilitated, and this facilitation, again, was dependent on beta-adrenergic activation. The data suggest that DG-LTP maintenance can be influenced by the BLA through different mechanisms: a short-lasting corticosterone-dependent and beta-adrenergic-independent mechanism and a long-lasting mechanism that facilitated hippocampal beta-adrenergic mechanisms.
机译：海马长时程增强（LTP）被广泛认为是学习和记忆形成的细胞模型。先前我们已经证明，通过短暂的急性游泳应激体验，持续约4-5小时的不依赖蛋白质合成的早期齿状回（DG）LTP可以转变为晚期LTP，持续时间> 24或= 24 h（高压力条件）。这种增强需要激活盐皮质激素受体和蛋白质合成。已知基底外侧杏仁核（BLA）通过β-肾上腺素能机制调节糖皮质激素对空间/上下文记忆巩固的作用。有趣的是，海马DG-LTP也可以通过β-肾上腺素能和胆碱能/毒蕈碱能过程间接调节。在这里，我们显示了在高应力条件下早期DG-LTP的增强取决于新型空间/上下文信息的处理。此外，与假手术和完整对照相比，这种增强在BLA病变动物中被阻断。然而，它不依赖于β-肾上腺素或胆碱能/毒蕈碱能受体的激活。相反，在低压力条件下，促进了BLA病变动物中晚期LTP的诱导，而这种促进作用又取决于β-肾上腺素的激活。数据表明，BLA可以通过不同的机制来影响DG-LTP的维持：一种短时的皮质酮依赖性和β-肾上腺素依赖性机制，以及一种促进海马β-肾上腺素机制的持久机制。

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