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Séminaire impromptu - Markus WohrUltrasonic Communication in Rodents: Genes, Brain and Behavior

Abstract :


 Mice and rats are highly social animals, with a rich social behavior repertoire, including the emission of so-called ultrasonic vocalizations (USV),
i.e. calls in the ultrasonic range above the human hearing threshold of about 20 kHz. In rats, typically three main types of USV can be distinguished based on a number of acoustic features, such as call duration, peak frequency, and frequency modulation: (I) Isolation-induced 40-kHz USV in pups, as well as (II) aversive 22-kHz USV and (III) appetitive 50-kHz USV in juvenile and adult rats. Specifically, 22-kHz USV occur in aversive situations, such as predator exposure and fighting, or during drug withdrawal, while 50-kHz USV occur in appetitive situations, such as rough-and-tumble play and mating, or in response to drugs of abuse, e.g. amphetamine.
Evidence from selective breeding, devocalization, and playback studies suggests that aversive 22-kHz USV and appetitive 50-kHz USV serve as situation-dependent socio-affective signals with distinct communicative functions, for instance 50-kHz USV as play signals and/ or social contact calls. While 22-kHz USV fulfill an alarming function and induce freezing behavior in the receiver, 50-kHz USV lead to social approach behavior.
These opposite behavioral responses are paralleled by distinct patterns of brain activation. Freezing behavior in response to 22-kHz USV is paralleled by increased neuronal activity in brain areas regulating fear and anxiety, such as amygdala and periaqueductal gray, whereas social approach behavior elicited by 50-kHz USV is accompanied by reduced activity levels in the amygdala, but enhanced activity in the nucleus accumbens, a brain area implicated in reward processing.
Affective ultrasonic communication offers therefore a translational tool to study the neurobiology underlying socio-affective communication. This is particularly relevant for rodent models of neurodevelopmental disorders characterized by social and communication deficits, such as autism.

Selected publications

Five Selected Publications (since 2014)
Mosienko M, Beis D, Alenina N, Wöhr M (2015) Reduced isolation-induced pup ultrasonic communication in mouse pups lacking brain serotonin. Molecular Autism 6:e13.

Valluy J, Bicker S, Aksoy-Aksel A, Lackinger M, Sumer S, Fiore R, Wüst T, Seffer D, Metge F, Dieterich C, Wöhr M, Schwarting RKW, Schratt GM (2015) A coding-independent function of an alternative Ube3a transcript during neuronal development. Nature Neuroscience 18:666-673.

Willuhn I, Tose A, Wanat MJ, Hart AS, Hollon NG, Phillips PEM, Schwarting RKW, Wöhr M (2014) Phasic dopamine release in the nucleus accumbens in response to pro-social 50-kHz ultrasonic vocalizations in rats. The Journal of Neuroscience 34:10616-10623.

Wöhr M (2014) Ultrasonic vocalizations in Shank mouse models for autism spectrum disorders: Detailed spectrographic analyses and developmental profiles. Neuroscience and Biobehavioral Reviews 43:199-212.

Wöhr M, Orduz D, Gregory P, Moreno H, Khan U, Vörckel KJ, Wolfer DP, Welzl H, Gall D, Schiffmann SN, Schwaller B (2015) Lack of parvalbumin in mice leads to behavioral deficits relevant to all human autism core symptoms and related neural morphofunctional abnormalities. Translational Psychiatry 5:e525.

Scientific focus :

My main research interests include neurobiological mechanisms underlying deficits in social behavior, acoustic communication through ultrasonic vocalizations, and socio-affective information processing in rodents. My team and I currently pursue two primary areas of research funded by the German Research Council (Deutsche Forschungsgemeinschaft, DFG). The first area of research investigates the distinct communicative functions of ultrasonic vocalizations in regulating social behavior in rodents. Here, we apply two main experimental approaches, focusing on sender and receiver, respectively. Firstly, we study the emission of ultrasonic vocalizations in the sender exposed to multiple social contexts differing in emotional valence, and validate their functional roles by means of surgical devocalization.
Secondly, we developed a playback paradigm, which allows us to assess behavioral responses elicited in the receiver, in combination with measurements of neurotransmitter release by fast-scan cyclic voltammetry or changes in neuronal activity patterns by electrophysiological recordings in freely-moving rodents.
A second line of research aims at the identification and translational cross-validation of genetic risk factors for ASD and SCZ in genetically-modified organisms, including rodents lacking genes encoding for transsynaptic and scaffolding proteins (e.g. Nlgn2 and Shank1) calcium signaling complexes (e.g. Cacna1c and Pvalb), and components involved in proper neurotransmitter functioning (e.g. Slc6a4 and Tph2).