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摘要 : 虽然叹气是呼吸和呼吸生理的一个有机组成部分,但我们对控制这一行为的神经回路却知之甚少。


虽然叹气是呼吸和呼吸生理的一个有机组成部分,但我们对控制这一行为的神经回路却知之甚少。在这项研究中,加州大学洛杉矶分校研究员Mark Krasnow及同事在髓质中识别出了一个小子类的、通过基因定义的神经元,它们投射到 呼吸节律发生器“preBötzinger complex” (preBötC)上,来驱动叹息。这一联系的抑制能完全消除叹气,而正常呼吸却不受影响。作者提出了一个机制,按照该机制,特定preBötC 神经元可能会对生理输入和可能的情绪输入进行整合,以便在适当的时候将普通呼吸转变成叹气。


The peptidergic control circuit for sighing


Sighs are long, deep breaths expressing sadness, relief or exhaustion. Sighs also occur spontaneously every few minutes to reinflate alveoli, and sighing increases under hypoxia, stress, and certain psychiatric conditions. Here we use molecular, genetic, and pharmacologic approaches to identify a peptidergic sigh control circuit in murine brain. Small neural subpopulations in a key breathing control centre, the retrotrapezoid nucleus/parafacial respiratory group (RTN/pFRG), express bombesin-like neuropeptide genes neuromedin B (Nmb) or gastrin-releasing peptide (Grp). These project to the preBötzinger Complex (preBötC), the respiratory rhythm generator, which expresses NMB and GRP receptors in overlapping subsets of ~200 neurons. Introducing either neuropeptide into preBötC or onto preBötC slices, induced sighing or in vitro sigh activity, wheras elimination or inhibition of either receptor reduced basal sighing, and inhibition of both abolished it. Ablating receptor-expressing neurons eliminated basal and hypoxia-induced sighing, but left breathing otherwise intact initially. We propose that these overlapping peptidergic pathways comprise the core of a sigh control circuit that integrates physiological and perhaps emotional input to transform normal breaths into sighs.

来源: Nature 浏览次数:1


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