Faculty Information |
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Article types | Original article |
Language | English |
Refereed paper | Refereed |
Title | The postnatal development of ultrasonic vocalization-associated breathing is altered in glycine transporter 2-deficient mice. |
Journal | Formal name:The Journal of physiology Abbreviation:J Physiol ISSN code:1469779300223751 |
Domestic / Foregin | Foregin |
Volume, Number, Page | 597(1),pp.173-191 |
International coauthorship | International coauthorship |
Papers・Author | Hülsmann Swen, Oke Yoshihiko, Mesuret Guillaume, Latal A Tobias, Fortuna Michal G, Niebert Marcus, Hirrlinger Johannes, Fischer Julia, Hammerschmidt Kurt |
Publication date | 2019/01 |
Papers・Description | KEY POINTS: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.ABSTRACT:Mouse models are instrumental with respect to determining the genetic basis and neural foundations of breathing regulation. To test the hypothesis that glycinergic synaptic inhibition is required for normal breathing and |
DOI | 10.1113/JP276976 |
PMID | 30296333 |