On the basis of the evidence that the basolateral amygdala (BLA) modulates hippocampal memory processes via synaptic plasticity, here we report that adrenergic β receptor activation in the BLA rescues amyloid β_1-42 (Aβ_1-42)-induced attenuation of long-term potentiation (LTP) at perforant pathway-dentate granule cell (DGC) synapses. When 500 μM isoproterenol (2 μl), an adrenergic β receptor agonist, was injected into the BLA 20 min before LTP induction, LTP was enhanced. Isoproterenol-mediated enhancement of LTP was blocked by co-injection with 100 μM ZnAF-2DA, an intracellular Zn²⁺ chelator, suggesting that intracellular Zn²⁺ is required for the intracellular signaling cascade after adrenergic β receptor activation in the BLA. Aβ_1-42-induced attenuation of LTP, which was induced by Aβ_1-42 injection into the dentate gyrus 60 min before LTP induction, was rescued by isoproterenol injection into the BLA 20 min before LTP induction, but not by 500 μM phenylephrine (2 μl), an adrenergic α₁ receptor agonist, injection into the BLA, which did not enhance LTP unlike the case of isoproterenol injection. Interestingly, Aβ_1-42-induced attenuation of LTP was also rescued by 100 μM isoproterenol injection into the BLA 20 min before LTP induction, which did not enhance LTP. The present study demonstrates that adrenergic β receptor activation in the BLA, which is linked with intracellular Zn²⁺ signaling, rescues Aβ_1-42-induced attenuation of dentate gyrus LTP. It is likely that adrenergic β receptor activation in the BLA is a strategy for rescuing Aβ_1-42-induced cognitive decline that is associated with hippocampal synaptic plasticity.

根据证据，基底外侧杏仁核（BLA）通过突触可塑性调节海马记忆过程，在此我们报道BLA中的肾上腺素β受体激活可以挽救淀粉样_β1-42（_Aβ1-42）诱导的长时程衰减。穿孔途径-齿状颗粒细胞（DGC）突触处的术语增强（LTP）。在诱导LTP之前20分钟，将500μM肾上腺素β受体激动剂异丙肾上腺素（2μl）注入BLA中，LTP增强。与100μM细胞内Zn ²⁺螯合剂ZnAF-2DA共同注射可阻止异丙肾上腺素介导的LTP增强，这表明在BLA中肾上腺素β受体激活后，细胞内信号级联反应需要细胞内Zn ²⁺。Aβ在LTP诱导前60分钟通过_Aβ1-42注射到齿状回中诱导_1-42诱导的LTP衰减，在LTP诱导前20分钟通过在BLA中注射异丙肾上腺素来挽救LTP的衰减，但不是通过500μM苯肾上腺素来挽救（2微升），肾上腺素能α ₁受体激动剂，注入BLA，这不增强LTP不像异丙肾上腺素注射的情况下。有趣的是，通过在LTP诱导前20分钟向BLA注射100μM异丙肾上腺素，也可以挽救_Aβ1-42诱导的LTP衰减，但不会增强LTP。本研究表明BLA中的肾上腺素β受体激活与细胞内Zn ²⁺信号传导有关，可以挽救_Aβ1-42诱导的齿状回LTP的衰减。BLA中的肾上腺素β受体激活可能是挽救_Aβ1-42诱导的与海马突触可塑性相关的认知功能减退的策略。