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Behavioral phenotyping devices have been successfully used to build ethograms, but many aspects of behavior remain out of reach of available phenotyping systems. We now report on a novel device, which consists in an open-field platform resting on highly sensitive piezoelectric (electromechanical) pressure-sensors, with which we could detect the slightest movements (up to individual heart beats during rest) from freely moving rats and mice. The combination with video recordings and signal analysis based on time-frequency decomposition, clustering, and machine learning algorithms provided non-invasive access to previously overlooked behavioral components. The detection of shaking/shivering provided an original readout of fear, distinct from but complementary to behavioral freezing. Analyzing the dynamics of momentum in locomotion and grooming allowed to identify the signature of gait and neurodevelopmental pathological phenotypes. We believe that this device represents a significant progress and offers new opportunities for the awaited advance of behavioral phenotyping.

This study analyzes the strategic use of public debt. Contrary to the classical view that politicians can use public debt to tie the hands of their successors, we show that an incumbent government can take advantage of having tied its own hands before the election with the help of public debt. By doing this, it reduces the basis for future social conflicts and benefits from social peace during its term, which may enhance its chances of being re-elected. In addition, in the case of foreign or external public debt, the incumbent can strategically divert future social conflicts toward a common enemy (foreign creditors). Thus, by increasing public debt before the election, the incumbent can strengthen social cohesion during his/her mandate, both by reducing the basis of internal conflicts and by diverting citizens from internal toward external rent-seeking activities.

Tauopathies, including Alzheimer's Disease, are the most frequent neurodegenerative diseases in elderly people and cause various cognitive, behavioural and motor defects, but also progressive language disorders. For communication and social interactions, mice produce ultrasonic vocalization (USV) via expiratory airflow through the larynx. We examined USV of Tau.P301L mice, a mouse model for tauopathy expressing human mutant tau protein and developing cognitive, motor and upper airway defects. At age 4-5 months, Tau.P301L mice had normal USV, normal expiratory airflow and no brainstem tauopathy. At age 8-10 months, Tau.P301L mice presented impaired USV, reduced expiratory airflow and severe tauopathy in the periaqueductal gray, Kolliker-Fuse and retroambiguus nuclei. Tauopathy in these nuclei that control upper airway function and vocalization correlates well with the USV impairment of old Tau.P301L mice. In a mouse model for tauopathy, we report for the first time an age-related impairment of USV that correlates with tauopathy in midbrain and brainstem areas controlling vocalization. The vocalization disorder of old Tau.P301L mice could be, at least in part, reminiscent of language disorders of elderly suffering tauopathy.

The variation in heart rate in phase with breathing, called respiratory sinus arrhythmia (RSA), is cardio-protective1,2. RSA amplitude provides an index of health and physical fitness used both clinically, and by the broader population using “smart” watches. Relaxation and positive socio-emotional states can amplify RSA3, yet the underlying mechanism remains largely unknown. Here, we identify a hypothalamus-brainstem neuronal network through which the neuromodulator oxytocin (OT), known for its relaxing and prosocial effects4, amplifies RSA during calming behavior. OT neurons from the caudal paraventricular nucleus in the hypothalamus were found to regulate the activity of a subgroup of inhibitory neurons in the pre-Bötzinger complex, the brainstem neuronal group that generates the inspiratory rhythm. Specifically, OT amplifies the inspiratory glycinergic input from pre-Bötzinger complex neurons to cardiac-innervating parasympathetic neurons in the nucleus ambiguus. This leads to amplified respiratory modulation of parasympathetic activity to the heart, thereby amplifying RSA. Behaviorally, OT neurons participate in the restoration of RSA amplitude during recovery from stress. This work shows how a central action of OT induces a physiologically beneficial regulation of cardiac activity during a calming behavior, providing a foundation for therapeutic strategies for anxiety disorders and coping with stress. Furthermore, it identifies a phenotypic signature of a subpopulation of neurons controlling RSA, namely pre-Bötzinger complex neurons expressing the OT-receptor, enabling the specific modulation of RSA amplitude to resolve its physiological and psychological functions.