Asset Details
Do you wish to reserve the book?
The peptidergic control circuit for sighing
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
The peptidergic control circuit for sighing
Do you wish to request the book?
The peptidergic control circuit for sighing
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
The peptidergic control circuit for sighing
2016
Overview
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.
The peptidergic neuronal circuit controlling sigh generation has been identified as ~200
Nmb-
or
Grp
-expressing neurons in the RTN/pFRG breathing control centre of the medulla that project to ~200 receptor-expressing neurons in the respiratory rhythm generator, the preBötzinger Complex.
Sigh centre neurons identified
Although sighs are an integral part of breathing and respiratory physiology, little is known about the neuronal circuits controlling this behaviour. Here, Mark Krasnow and colleagues identify a small subset of genetically defined neurons in the medulla that project to the preBötzinger complex (preBötC), the respiratory rhythm generator, to drive sighing. Inhibition of this connection could completely eliminate sighs, while regular breathing was left intact. The authors propose a mechanism by which specific preBötC neurons may integrate physiological and possibly emotional inputs to turn regular breaths into sighs when appropriate.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Animals
/ Bombesin
/ Complications and side effects
/ Female
/ Gastrin
/ Gastrin-Releasing Peptide - deficiency
/ Gastrin-Releasing Peptide - genetics
/ Gastrin-Releasing Peptide - metabolism
/ Humanities and Social Sciences
/ Hypoxia
/ Male
/ Mice
/ Neurokinin B - analogs & derivatives
/ Rats
/ Receptors, Bombesin - metabolism
/ Respiratory Center - cytology
/ Respiratory Center - drug effects
/ Respiratory Center - physiology
/ Ribosome Inactivating Proteins, Type 1 - pharmacology
/ Rodents
/ Saporins
/ Science
/ Signal Transduction - drug effects
