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β-Adrenergic facilitation of synaptic plasticity in the rat basolateral amygdala in vitro is gradually reversed by corticosterone

机译:β-肾上腺素促进大鼠基底外侧杏仁核突触可塑性在体外被皮质酮逆转

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摘要

The rat basolateral amygdala is important for emotional learning; this is modulated by noradrenaline and corticosterone. We report that the β-adrenergic agonist isoproterenol markedly enhances synaptic plasticity induced in the basolateral amygdala by a weak stimulation paradigm but is ineffective with stronger protocols. Simultaneous application of corticosterone gradually reversed the facilitatory effect of isoproterenol. When corticosterone was briefly applied several hours prior to isoproterenol, facilitatory effects of the β-agonist were entirely suppressed. This suggests that in the basolateral amygdala, β-adrenergic influences promote synaptic plasticity; this is gradually normalized by corticosterone, preventing the network from overshooting.
机译:大鼠基底外侧杏仁核对情绪学习很重要。这是由去甲肾上腺素和皮质酮调节的。我们报告说,β-肾上腺素能激动剂异丙肾上腺素能明显增强通过弱刺激范式在基底外侧杏仁核中诱导的突触可塑性,但对于更强的方案无效。皮质酮的同时应用逐渐逆转了异丙肾上腺素的促进作用。当在异丙肾上腺素之前数小时短暂应用皮质酮时,β-激动剂的促进作用被完全抑制。这表明在基底外侧杏仁核中,β-肾上腺素能促进突触可塑性。皮质酮逐步将其标准化,防止网络超调。

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