Cui Yan, Bondarenko Evgeny, Thörn Perez Carolina, Chiu Delia N, Feldman Jack L
Department of Physiology, Chengdu Medical College, Chengdu, China.
Department of Neurobiology, DGSOM, UCLA, Los Angeles, United States.
Elife. 2025 Jun 24;13:RP100192. doi: 10.7554/eLife.100192.
We explored neural mechanisms underlying sighing in mice. Photostimulation of parafacial (pF) neuromedin B (NMB) or gastrin-releasing peptide (GRP), or preBötzinger Complex (preBötC) NMBR or GRPR neurons elicited ectopic sighs with latency inversely related to time from preceding endogenous sigh. Of particular note, ectopic sighs could be produced without involvement of these peptides or their receptors in preBötC. Moreover, chemogenetic or optogenetic activation of preBötC SST neurons induced sighing, even in the presence of NMBR and/or GRPR antagonists. We propose that an increase in the excitability of preBötC NMBR or GRPR neurons not requiring activation of their peptide receptors activates partially overlapping pathways to generate sighs, and that preBötC SST neurons are a downstream element in the sigh generation circuit that converts normal breaths into sighs.
我们探究了小鼠叹气背后的神经机制。对面部旁（pF）神经介素B（NMB）或胃泌素释放肽（GRP），或前包钦格复合体（preBötC）中的NMBR或GRPR神经元进行光刺激，会引发异位叹气，其潜伏期与距前一次内源性叹气的时间呈负相关。特别值得注意的是，在不涉及这些肽或它们在前包钦格复合体中的受体的情况下也能产生异位叹气。此外，即使存在NMBR和/或GRPR拮抗剂，对前包钦格复合体SST神经元进行化学遗传或光遗传激活也会诱发叹气。我们提出，前包钦格复合体NMBR或GRPR神经元兴奋性的增加，无需其肽受体的激活，就能激活部分重叠的通路来产生叹气，并且前包钦格复合体SST神经元是叹气产生回路中的一个下游元件，可将正常呼吸转换为叹气。
