The lateral parabrachial nucleus (LPBN) is known to relay noxious information to the amygdala for processing affective responses. However, it is unclear whether the LPBN actively processes neuropathic pain characterized by persistent hyperalgesia with aversive emotional responses. Here we report that neuropathic pain-like hypersensitivity induced by common peroneal nerve (CPN) ligation increases nociceptive stimulation-induced responses in glutamatergic LPBN neurons. Optogenetic activation of GABAergic LPBN neurons does not affect basal nociception, but alleviates neuropathic pain-like behavior. Optogenetic activation of glutamatergic or inhibition of GABAergic LPBN neurons induces neuropathic pain-like behavior in naïve mice. Inhibition of glutamatergic LPBN neurons alleviates both basal nociception and neuropathic pain-like hypersensitivity. Repetitive pharmacogenetic activation of glutamatergic or GABAergic LPBN neurons respectively mimics or prevents the development of CPN ligation-induced neuropathic pain-like hypersensitivity. These findings indicate that a delicate balance between excitatory and inhibitory LPBN neuronal activity governs the development and maintenance of neuropathic pain.

已知臂外侧臂旁核（LPBN）将有害信息传递给杏仁核，以处理情感反应。但是，尚不清楚LPBN是否能积极处理以持续性痛觉过敏为特征的厌恶性情绪反应。在这里，我们报道由腓总神经（CPN）结扎引起的神经性疼痛样超敏反应增加了谷氨酸能LPBN神经元的伤害性刺激诱导反应。GABA能LPBN神经元的光遗传激活不影响基础伤害感受，但可以减轻神经性疼痛样行为。谷氨酸能的光遗传激活或GABA能的LPBN神经元的抑制会在幼稚的小鼠中诱发神经性疼痛样行为。抑制谷氨酸能LPBN神经元可减轻基础伤害感受和神经性疼痛样超敏反应。谷氨酸能或GABA能的LPBN神经元的重复药理学激活分别模拟或阻止CPN结扎诱导的神经性疼痛样超敏反应的发展。这些发现表明，兴奋性和抑制性LPBN神经元活性之间的微妙平衡决定了神经性疼痛的发生和维持。