Helmholtz Gemeinschaft

Search
Browse
Statistics
Feeds

Genetic identification of a hindbrain nucleus essential for innate vocalization

Item Type:Article
Title:Genetic identification of a hindbrain nucleus essential for innate vocalization
Creators Name:Hernandez-Miranda, L.R., Ruffault, P.L., Bouvier, J.C., Murray, A.J., Morin-Surun, M.P., Zampieri, N., Cholewa-Waclaw, J.B., Ey, E., Brunet, J.F., Champagnat, J., Fortin, G. and Birchmeier, C.
Abstract:Vocalization in young mice is an innate response to isolation or mechanical stimulation. Neuronal circuits that control vocalization and breathing overlap and rely on motor neurons that innervate laryngeal and expiratory muscles, but the brain center that coordinates these motor neurons has not been identified. Here, we show that the hindbrain nucleus tractus solitarius (NTS) is essential for vocalization in mice. By generating genetically modified newborn mice that specifically lack excitatory NTS neurons, we show that they are both mute and unable to produce the expiratory drive required for vocalization. Furthermore, the muteness of these newborns results in maternal neglect. We also show that neurons of the NTS directly connect to and entrain the activity of spinal (L1) and nucleus ambiguus motor pools located at positions where expiratory and laryngeal motor neurons reside. These motor neurons control expiratory pressure and laryngeal tension, respectively, thereby establishing the essential biomechanical parameters used for vocalization. In summary, our work demonstrates that the NTS is an obligatory component of the neuronal circuitry that transforms breaths into calls.
Keywords:Vocalization, Expiration, Hindbrain, Premotor Neurons, Olig3, Animals, Mice
Source:Proceedings of the National Academy of Sciences of the United States of America
ISSN:0027-8424
Publisher:National Academy of Sciences
Volume:114
Number:30
Page Range:8095-8100
Date:25 July 2017
Official Publication:https://doi.org/10.1073/pnas.1702893114
External Fulltext:View full text on PubMed Central
PubMed:View item in PubMed

Repository Staff Only: item control page

Open Access
MDC Library