The peptidergic control circuit for sighing.
Author: Li P#1, Janczewski WA#2, Yackle K#1, Kam K2, Pagliardini S2, Krasnow MA1, Feldman JL2
Affiliation:
1Department of Biochemistry and Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA, 94305.
2Systems Neurobiology Laboratory, Department of Neurobiology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, 90095.
#Contributed equally
Conference/Journal: Nature.
Date published: 2016 Feb 18
Other:
Volume ID: 530 , Issue ID: 7590 , Pages: 293-297 , Special Notes: doi: 10.1038/nature16964. Epub 2016 Feb 8. , Word Count: 181
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, whereas 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.
PMID: 26855425 PMCID: PMC4852886 DOI: 10.1038/nature16964
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