Abstract

BackgroundRodent ultrasonic vocalizations (USVs) are crucial to their social communication and a widely used translational tool for linking gene mutations to behavior. To maximize the causal interpretation of experimental treatments, we need to understand how neural control affects USV production. However, both the aerodynamics of USV production and its neural control remain poorly understood.ResultsHere, we test three intralaryngeal whistle mechanisms—the wall and alar edge impingement, and shallow cavity tone—by combining in vitro larynx physiology and individual-based 3D airway reconstructions with fluid dynamics simulations. Our results show that in the mouse and rat larynx, USVs are produced by a glottal jet impinging on the thyroid inner wall. Furthermore, we implemented an empirically based motor control model that predicts motor gesture trajectories of USV call types.ConclusionsOur results identify wall impingement as the aerodynamic mechanism of USV production in rats and mice. Furthermore, our empirically based motor control model shows that both neural and anatomical components contribute to USV production, which suggests that changes in strain specific USVs or USV changes in disease models can result from both altered motor programs and laryngeal geometry. Our work provides a quantitative neuromechanical framework to evaluate the contributions of brain and body in shaping USVs and a first step in linking descending motor control to USV production.

Highlights

  • Rodent ultrasonic vocalizations (USVs) are crucial to their social communication and a widely used translational tool for linking gene mutations to behavior

  • We show that USVs are produced with adducted vocal folds, that only the wall impingement model predicts anatomically correct glottal air jet parameters, and that normal USVs are produced in absence of the alar edge and ventral pouch

  • We tested three physiological boundary conditions that are distinctive between wall and alar edge tone models for USV production: (i) vocal fold adduction state, (ii) jet separation and impingement locations, and (iii) the presence of the alar edge and ventral pouch cavity

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Summary

Introduction

Rodent ultrasonic vocalizations (USVs) are crucial to their social communication and a widely used translational tool for linking gene mutations to behavior. Translating motor control to USV production requires both system identification of the mechanism by which sound is produced and quantitative understanding of how muscles drive the control parameters of this system. The impingement structure within the larynx has been proposed to be either the thyroid wall [26] or a laryngeal adaptation [28] found in several muroid rodents, the alar edge [28, 29] (Fig. 1) Both mechanisms constrain motor control to the respiratory and laryngeal musculature, but the proposed aeroacoustic models for wall and alar edge tones occur under distinct physiological conditions and predict very different sound frequencies [26, 28]. Establishing which aerodynamic mechanism is responsible for USV production is critical for quantitatively linking neuromuscular control parameters to USV acoustics

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