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首页> 外文期刊>The European Journal of Neuroscience >Favouring inhibitory synaptic drive mediated by GABA(A) receptors in the basolateral nucleus of the amygdala efficiently reduces pain symptoms in neuropathic mice
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Favouring inhibitory synaptic drive mediated by GABA(A) receptors in the basolateral nucleus of the amygdala efficiently reduces pain symptoms in neuropathic mice

机译：杏仁核基底外侧核中由GABA（A）受体介导的抑制性突触驱动有效降低神经性小鼠的疼痛症状

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摘要

Pain is an emotion and neuropathic pain symptoms are modulated by supraspinal structures such as the amygdala. The central nucleus of the amygdala is often called the nociceptive amygdala', but little is known about the role of the basolateral amygdala. Here, we monitored the mechanical nociceptive thresholds in a mouse model of neuropathic pain and infused modulators of the glutamate/GABAergic transmission in the basolateral nucleus of the amygdala (BLA) via chronically-implanted cannulas. We found that an N-methyl-D-aspartate-type glutamate receptor antagonist (MK-801) exerted a potent antiallodynic effect, whereas a transient allodynia was induced after perfusion of bicuculline, a GABA(A) receptor antagonist. Potentiating GABA(A) receptor function using diazepam or etifoxine (a non-benzodiazepine anxiolytic) fully but transiently alleviated mechanical allodynia. Interestingly, the antiallodynic effect of etifoxine disappeared in animals that were incapable of producing 3-steroids. Diazepam had a similar effect but of shorter duration. As indicated by patch-clamp recordings of BLA neurons, these effects were mediated by a potentiation of GABA(A) receptor-mediated synaptic transmission. Together with a presynaptic elevation of miniature inhibitory postsynaptic current frequency, the duration and amplitude of GABA(A) miniature inhibitory postsynaptic currents were also increased (postsynaptic effect). The analgesic contribution of endogenous neurosteroid seemed to be exclusively postsynaptic. This study highlights the importance of the BLA and the local inhibitory/excitatory neuronal network activity while setting the mechanical nociceptive threshold. Furthermore, it appears that promoting inhibition in this specific nucleus could fully alleviate pain symptoms. Therefore, the BLA could be a novel interesting target for the development of pharmacological or non-pharmacological therapies.
机译：疼痛是一种情绪，而神经上的疼痛症状则由诸如杏仁核的棘上结构调节。杏仁核的中央核通常被称为伤害性杏仁核，但对基底外侧杏仁核的作用知之甚少。在这里，我们监测了小鼠的神经性疼痛模型中的机械伤害阈值，并通过长期植入的插管在杏仁核（BLA）的基底外侧核中注入了谷氨酸/ GABA能传递的调节剂。我们发现，N-甲基-D-天冬氨酸型谷氨酸受体拮抗剂（MK-801）发挥了有效的抗痛觉过敏作用，而在灌注小分子GABA（A）受体拮抗剂后诱发了短暂性痛觉过敏。使用地西epa或依替福辛（一种非苯二氮杂类抗焦虑药）可增强GABA（A）受体功能，但可暂时缓解机械性异常性疼痛。有趣的是，在不能产生3-类固醇的动物中，依替福星的抗痛觉过敏作用消失了。地西p具有相似的作用，但持续时间较短。正如BLA神经元的膜片钳记录所表明的那样，这些作用是通过增强GABA（A）受体介导的突触传递来介导的。随着微型抑制突触后电流频率的突触前升高，GABA（A）微型抑制突触后电流的持续时间和幅度也增加了（突触后效应）。内源性神经类固醇的止痛作用似乎完全是突触后的。这项研究突出了BLA和局部抑制性/兴奋性神经元网络活动的重要性，同时设置了机械伤害阈值。此外，似乎在该特定核中促进抑制可以完全缓解疼痛症状。因此，BLA可能成为药理学或非药理学治疗发展的一个新的有趣目标。

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