The postnatal development of ultrasonic vocalization-associated breathing is altered in glycine transporter 2-deficient mice

2019 | journal article. A publication with affiliation to the University of Göttingen.

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​The postnatal development of ultrasonic vocalization-associated breathing is altered in glycine transporter 2-deficient mice​
Hülsmann, S. ; Oke, Y.; Mesuret, G.; Latal, A. T.; Fortuna, M. G. ; Niebert, M.   & Hirrlinger, J.  et al.​ (2019) 
The Journal of Physiology597(1) pp. 173​-191​.​ DOI: https://doi.org/10.1113/JP276976 

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Authors
Hülsmann, Swen ; Oke, Yoshihiko; Mesuret, Guillaume; Latal, A. Tobias; Fortuna, Michal G. ; Niebert, Marcus ; Hirrlinger, Johannes ; Fischer, Julia ; Hammerschmidt, Kurt 
Abstract
Newborn mice produce ultrasonic vocalization to communicate with their mother. The neuronal glycine transporter (GlyT2) is required for efficient loading of synaptic vesicles in glycinergic neurons. Mice lacking GlyT2 develop a phenotype that resembles human hyperekplexia and the mice die in the second postnatal week. In the present study, we show that GlyT2-knockout mice do not acquire adult ultrasonic vocalization-associated breathing patterns. Despite the strong impairment of glycinergic inhibition, they can produce sufficient expiratory airflow to produce ultrasonic vocalization. Because mouse ultrasonic vocalization is a valuable read-out in translational research, these data are highly relevant for a broad range of research fields.
Issue Date
2019
Journal
The Journal of Physiology 
ISSN
0022-3751; 1469-7793
eISSN
1469-7793
Language
English

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