Persistent nociception induces anxiety-like behavior in rodents: role of endogenous neuropeptide S.
Persistent nociception induces anxiety-like behavior in rodents: role of endogenous neuropeptide S.
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DOI：
10.1016/j.pain.2014.04.026
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发表时间：
2014-08
期刊：
影响因子：
7.4
通讯作者：
Mao J
中科院分区：
文献类型：
--
作者：
Zhang S;Jin X;You Z;Wang S;Lim G;Yang J;McCabe M;Li N;Marota J;Chen L;Mao J
焦虑症是一种慢性疼痛的共病状态。容易上瘾和滥用的止痛药和抗焦虑药目前被用来控制疼痛和焦虑症状。然而，慢性疼痛和焦虑相互作用的细胞机制仍有待阐明。我们报道，周围神经损伤后持续的伤害性感觉在啮齿类动物中引起焦虑样行为。在伤害性行为和焦虑性行为共存的啮齿动物中，神经肽S(NPS)的表达和释放减少。脑室注射外源性NPS可同时改善伤害性行为和焦虑性行为。在细胞水平上，NPS通过增加中间神经元突触前GABA的释放来增强杏仁核内的抑制性传递。这些发现表明，啮齿动物伤害性行为和类焦虑行为之间的相互作用可能受到杏仁核内GABA能抑制的调节。这些数据表明，增强大脑NPS功能可能是管理共存的疼痛和焦虑的一种新策略。
Anxiety disorder is a comorbid condition of chronic pain. Analgesics and anxiolytics, subject to addiction and abuse, are currently used to manage pain and anxiety symptoms. However, the cellular mechanism underlying chronic pain and anxiety interaction remains to be elucidated. We report that persistent nociception following peripheral nerve injury induced anxiety-like behavior in rodents. Brain expression and release of neuropeptide S (NPS), a proposed endogenous anxiolytic peptide, was diminished in rodents with co-existing nociceptive and anxiety-like behaviors. Intracerebroventricular administration of exogenous NPS concurrently improved both nociceptive and anxiety-like behaviors. At the cellular level, NPS enhanced intra-amygdaloidal inhibitory transmission by increasing presynaptic GABA release from interneurons. These findings indicate that the interaction between nociceptive and anxiety-like behaviors in rodents may be regulated by the altered NPS-mediated intra-amygdaloidal GABAergic inhibition. The data suggest that enhancing the brain NPS function may be a new strategy to manage comorbid pain and anxiety.
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