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首页> 外文期刊>The European Journal of Neuroscience >Alpha2-adrenoreceptor activation inhibits LTP and LTD in the basolateral amygdala: involvement of Gi/o-protein-mediated modulation of Ca2+-channels and inwardly rectifying K+-channels in LTD.
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Alpha2-adrenoreceptor activation inhibits LTP and LTD in the basolateral amygdala: involvement of Gi/o-protein-mediated modulation of Ca2+-channels and inwardly rectifying K+-channels in LTD.

机译：Alpha2-肾上腺素受体激活抑制基底外侧杏仁核的LTP和LTD：参与Gi / o蛋白介导的Ca2 +通道的调节并向内纠正LTD中的K +通道。

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摘要

Activation of adrenoreceptors modulates synaptic transmission in the basolateral amygdala. Here, we investigated the effects of alpha2-adrenoreceptor activation on long-term depression and long-term potentiation in an in vitro slice preparation of the mouse basolateral amygdala. Field potentials and excitatory postsynaptic currents were evoked in the basolateral amygdala by stimulating the lateral amygdala. Norepinephrine (20 micro m) reduced synaptic transmission and completely blocked the induction of long-term potentiation and long-term depression. The alpha2-adrenoreceptor antagonist yohimbine (2 micro m) reversed this effect. The alpha2-adrenoreceptor agonist clonidine (10 micro m) mimicked the effects of norepinephrine. The Gi/o-protein inhibitor pertussis toxin (5 micro g/mL) reversed the effect of clonidine. Long-term depression was blocked in the presence of omega-conotoxin GVIA, but not omega-agatoxin IVA. Clonidine inhibited voltage-activated Ca2+ currents mediated via N- or P/Q-type Ca2+-channels. The inhibitory action of clonidine on long-term depression was reversed when inwardly rectifying K+-channels were blocked by Ba2+ (300 micro m). The present data suggest that alpha2-adrenoreceptor activation impairs the induction of long-term depression in the basolateral amygdala by a Gi/o-protein-mediated inhibition of presynaptic N-type Ca2+-channels and activation of inwardly-rectifying K+-channels.
机译：肾上腺素受体的激活调节基底外侧杏仁核中的突触传递。在这里，我们调查了小鼠基底外侧杏仁核的体外切片制备中α2-肾上腺素受体激活对长期抑郁和长期增强的影响。通过刺激外侧杏仁核，在基底外侧杏仁核中诱发出场电位和兴奋性突触后电流。去甲肾上腺素（20微米）减少了突触传递，并完全阻止了长期增强和长期抑郁的诱导。 α2肾上腺素受体拮抗剂育亨宾（2微米）逆转了这种作用。 α2-肾上腺素受体激动剂可乐定（10微米）模仿去甲肾上腺素的作用。 Gi / o蛋白抑制剂百日咳毒素（5 micro g / mL）逆转了可乐定的作用。在存在ω-芋螺毒素GVIA的情况下阻止了长期抑郁，但没有ω-藻毒素IVA的存在。可乐定抑制了通过N型或P / Q型Ca2 +通道介导的电压激活的Ca2 +电流。当向内整流的K +通道被Ba2 +（300 microm）阻断时，可乐定对长期抑郁的抑制作用被逆转。目前的数据表明，α2-肾上腺素受体的激活通过Gi / o蛋白介导的突触前N型Ca 2+通道的抑制和向内整流的K +通道的激活而损害了基底外侧杏仁核的长期抑制。

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