For much of childhood, limited metabolic resources are unevenly distributed between brain and body, with neural maturation prioritized over physical growth. This energy trade-off critically shapes language acquisition, a cornerstone of human development. The PhD project investigates whether disruptions in this brain–body balance contribute to developmental language disorder (DLD). Combining behavioral, EEG, and MRI measures in 150 children aged 4–7, it will examine how energy allocation influences predictive speech coordination—the ability to synchronize one’s voice with rhythmic sounds—and its neural basis in beta–gamma oscillatory coupling. Body growth trajectories (BMI) and brain metabolic activity during speech perception will serve as complementary indices of the energy trade-off. The project aims to reveal how atypical energy allocation alters neural efficiency and compromises language development.

The vestibular system is essential to ensure proper balance, postural control and gaze stabilization. In vertebrates, brainstem vestibular efferent neurons project bilaterally back to the inner ear where they synapse on all hair cells. Until now however, the role of the vestibular efferent system (EVS) has remained undetermined. In this proposal, we investigate the following hypothesis: (i) EVS would differentially modulate vestibular activity in passive and active contexts. (ii) EVS could participate to rebalance the vestibular system in pathological situations.
The results of these studies have significant implications for rehabilitation strategies leveraging spinal circuit plasticity.

The vestibular system is a multimodal sensory motor system essential for postural stabilization, gaze control and spatial orientation. Within vertebrates, a brainstem efferent vestibular system (EVS) provides bilateral projections to the labyrinth, where efferent axons establish synaptic contacts with both type I and type II hair cells, as well as with vestibular afferent calyces and bouton terminals. While this circuitry is anatomically conserved across vertebrate taxa, its physiological role in mammals remains insufficiently resolved. Classical hypotheses propose that the EVS regulates receptor sensitivity, adjusts afferent firing dynamics, and participates in activity-dependent plasticity of peripheral vestibular encoding. However, direct causal evidence is scarce.
This PhD project targets a central working hypothesis: the EVS provides behavior-dependent modulation of peripheral vestibular output. During development, the EVS might participate to the calibration of vestibular sensori-motor reflex by adjusting the tuning of peripheral inputs. In addition, efferent feedback may dynamically adjust the gain of vestibular transduction during active behaviour, thereby improving sensorimotor performance when head movements increase. In pathological situations, efferent signaling may contribute to compensatory rebalancing in conditions of asymmetric input, such as unilateral vestibular lesions. Identifying such mechanisms would redefine the vestibular periphery as an active, state-dependent processing stage rather than a purely feed-forward sensory element.
Our recent work in rodents demonstrated that activation of spinal central pattern generators (CPGs) facilitates spino-ocular coupling during locomotion. These data parallel observations in Xenopus in which swim-driven CPG discharges modulate vestibular afferents via efferent pathways. Although the precise sources of inputs to mammalian EVS neurons are incompletely mapped, evidence suggests direct projections from spinal locomotor circuits to brainstem efferent nuclei. Our preliminary data in mice indicate a significant enhancement of vestibulo-ocular reflex (VOR) gain during running. The latency and magnitude of this modulation are compatible with rapid efferent-mediated alterations of hair cell or afferent terminal excitability, mediated by cholinergic receptors expressed peripherally.
The proposed research will combine anatomical, physiological and behavioral approaches to determine whether CPG-mediated modulation of EVS neurons causally drives locomotion-dependent changes in VOR gain. First, monosynaptic and polysynaptic projections to EVS neurons will be characterized using anatomical tracers and immunohistochemical markers defining neurotransmitter identity. This will allow localization of spinal or supraspinal neurons projecting to efferent nuclei and quantification of projection density along the rostrocaudal axis.
Next, efferent modulation at the labyrinth will be perturbed using transtympanic delivery of pharmacological agents targeting specific nicotinic receptors, muscarinic receptors, or associated modulatory pathways. Behavioral VOR responses will be quantified in behaving mice, while eye movements will be recorded at high temporal resolution. By systematically varying behavioural context and pharmacological conditions, we will determine whether VOR gain modulation scales with CPG output and whether it is modulated by EVS activity.
In parallel, in vivo calcium imaging of identified EVS neurons will allow real-time assessment of efferent recruitment during locomotion.
This integrative framework will provide the first causal demonstration, in mammals, that the EVS is a behavior-dependent sensory control system allowing rapid modulation of labyrinthine encoding. Such findings would significantly advance vestibular neuroscience by linking locomotor CPG output, efferent brainstem circuits, and peripheral sensory tuning. From a translational perspective, the results may open new avenues for rehabilitation after unilateral vestibular hypofunction, exploiting spinal circuit plasticity or pharmacological targeting of efferent pathways to restore vestibular function.

This PhD project will investigate how the auditory thalamocortical circuit contributes accurate to learning and perception by examining its synaptic plasticity and dynamic regulation during behavior. Using two-photon calcium imaging in mice performing auditory discrimination tasks, we will track activity in thalamic inputs and cortical neurons across different learning stages to reveal how experience shapes circuit function. A schizophrenia pathology–related mouse model will be used to identify alterations in thalamocortical communication associated with impaired perception. In a second phase, targeted modulation of thalamic activity will test its causal influence on cortical plasticity and behavioral adaptation. Together, these studies will uncover fundamental principles governing how thalamic input drives cortical learning, providing mechanistic insight into the cellular basis of adaptive cognition.

Background and Rationale
Learning and memory rely on the brain’s capacity to modify synaptic connections and dynamically adjust information flow across cortical and subcortical networks. The thalamus plays a critical role in these processes by regulating how sensory signals are integrated, filtered, and relayed to cortical areas. Beyond its traditional role as a sensory gateway, the thalamus participates actively in higher-order functions such as associative learning, contextual modulation, and cognitive flexibility.
Within the auditory system, the secondary auditory thalamocortical (2ATC) pathway — linking the auditory thalamus (AT) with the secondary auditory cortex (2AC) — is a central hub for integrating sensory experience with learned associations. This circuit also communicates extensively with limbic and frontal regions, positioning it as a key structure for transforming perceptual input into memory and decision-relevant representations.
Alterations in thalamocortical communication and excitatory–inhibitory balance have been observed in several conditions associated with impaired sensory integration and cognitive deficits, including schizophrenia. Understanding the synaptic and circuit mechanisms that underlie these disturbances could inform strategies for circuit-level interventions, but fundamental questions remain about how thalamocortical plasticity supports normal learning and memory processes.
This project will therefore investigate how activity-dependent plasticity within the auditory thalamocortical circuit contributes to associative learning, and how its disruption in a schizophrenia pathology–related mouse model affects information processing and behavioral adaptation.

Hypotheses and Objectives
We hypothesize that the auditory thalamocortical circuit exhibits bidirectional plasticity that encodes learning-related changes in stimulus–outcome associations, and that disruption of this mechanism leads to altered sensory and cognitive performance. We further propose that targeted modulation of thalamic input can influence cortical plasticity and behavioral outcomes, revealing causal links between thalamic dynamics and learning efficacy.
To address these hypotheses, the project is organized into two experimental aims.

Aim 1 – Characterizing Thalamocortical Plasticity During Auditory Learning
The first aim seeks to define how synaptic and circuit-level plasticity within the 2ATC pathway evolves during associative learning. Mice will be trained in an auditory Go/No-Go discrimination task where specific tones predict rewarding or aversive outcomes. Using two-photon calcium imaging, we will record activity from presynaptic boutons of thalamic projections and postsynaptic dendrites of cortical neurons during task performance.
This approach will allow longitudinal tracking of structural and functional plasticity across different phases of learning — acquisition, consolidation, and reversal. By comparing activity patterns between control animals and a schizophrenia pathology–related mouse model, we will determine how changes in synaptic strength and coordination reflect learning performance and memory flexibility.
The analysis will focus on how thalamic inputs shape cortical representations over time, and how their modulation corresponds to behavioral indices such as discrimination accuracy, response latency, and learning speed. These results will establish a cellular and functional map of thalamocortical plasticity during auditory learning.

Aim 2 – Causal Modulation of Thalamic Activity and Its Impact on Learning and Plasticity
The second aim will test the causal contribution of thalamic activity to cortical plasticity and learning behavior. To this end, we will combine two-photon imaging with focal electrical stimulation of the auditory thalamus during behavior.
By systematically varying stimulation timing and frequency, we will assess how enhanced or suppressed thalamic drive influences cortical dynamics and behavioral performance. Longitudinal imaging will reveal whether specific patterns of thalamic activation can promote functional synaptic remodeling in the auditory cortex, thereby accelerating or stabilizing learning.
In parallel, we will compare these effects between control and schizophrenia pathology–related models to determine whether circuit-level interventions can compensate for impaired plasticity. This aim will thus provide mechanistic insight into how thalamic input regulates cortical learning rules and whether this regulation remains flexible under altered network conditions.

Expected Outcomes and Significance
This project will elucidate fundamental principles of thalamocortical plasticity in learning and memory. Specifically, it will:
1. Define how coordinated synaptic changes in the auditory thalamocortical circuit underlie associative learning.
2. Identify how circuit dysfunction affects sensory–cognitive integration in a validated model of schizophrenia-related pathology.
3. Establish causal evidence that modulation of thalamic activity can influence cortical plasticity and behavioral adaptation.
Beyond its relevance to auditory processing, the project will contribute broadly to our understanding of how thalamic circuits support flexible learning and memory formation. These findings may also provide a mechanistic foundation for future circuit-based interventions targeting cognitive and perceptual disturbances, though the primary focus remains on basic neurophysiological mechanisms.