Biology subjects

Cattaert, D.

Publications and source records attributed to Cattaert, D..

4 recordsLinked to original sources

bioRxiv2026

Differential maturation in vestibular neuronal groups related to developmental motor reorganization in amphibians

Vestibular neurons are core elements of the pathways involved in vestibulo-motor functions, such as vestibulo-spinal and vestibulo-ocular reflexes. To meet behavioral needs, electrophysiological neuronal properties are adequately adapted to the sensory-motor computation sustaining these distinct vestibular reflexes. During frog metamorphosis, there is a complete reorganization of the posturo-locomotor system while the oculomotor system remains minimally changed, probably associated to so far unknown changes in vestibular neuronal properties. We used this unique model to investigate the central developmental mechanisms underlying such a reconfiguration of vestibular-associated behaviors. Central vestibular neurons exhibit two types of electrophysiological phenotypes: tonic neurons with a continuous discharge and phasic neurons with a transitory discharge mainly due to the activation of Kv1.1 channel. Electrophysiological recordings and Kv1.1 immunolabeling of vestibulospinal (VS) and vestibulo-ocular (VO) neurons at both larval and juvenile stages revealed that the majority of VS neurons exhibited a tonic discharge in larvae but a phasic discharge in juvenile, while VO neurons remained mainly tonic throughout development. Changes in phasic and tonic neurons proportions in VS population are partly explained by neurogenesis. But we provide evidences that an electrophysiological phenotype switch is a concomitant developmental mechanism participating in the maturation of these central vestibular neurons. All together our results showed that the maturation process in central vestibular neuronal groups is highly related to the metamorphosis-induced remodeling of vestibulo-motor functions they are involved in, with the ultimate purpose of ensuring an adequate adaptation of neuronal elements properties to the developmental changes of behavioral constrains.

neuroscience↗

bioRxiv2023

Role of spinal sensorimotor circuits in triphasic command: a simulation approach using Goal Exploration Process

During rapid voluntary limb movement about a single joint, a stereotyped triphasic pattern is typically observed in the electromyograms (EMGs) of antagonistic muscles acting at this joint. To explain the origin of such triphasic commands, two types of theories have been proposed. Peripheral theories consider that triphasic commands result from sensorimotor spinal networks, either through a combination of reflexes or through a spinal central pattern generator. Central theories consider that the triphasic command is elaborated in the brain. Although both theories were partially supported by physiological data, there is still no consensus about how exactly triphasic commands are elaborated. Moreover, capacities of simple spinal sensorimotor circuits to elaborate triphasic commands on their own have not been tested yet. In order to test this, we modelled arm musculoskeletal system, muscle activation dynamics, proprioceptive spindle and Golgi afferent activities and spinal sensorimotor circuits. Step commands were designed to modify the activity of spinal neurons and the strength of their synapses, either to prepare (SET) the network before movement onset, or to launch the movement (GO). Since these step commands do not contain any dynamics, changes in muscle activities responsible for arm movement rest entirely upon interactions between the spinal network and the musculo-skeletal system. Critically, we selected step commands using a Goal Exploration Process inspired from baby babbling during development. In this task, the Goal Exploration Process proved very efficient at discovering step commands that enabled spinal circuits to handle a broad spectrum of functional behaviors, displayed in a behavioral space characterized by movement amplitude and maximal speed. All over the behavioral space, specific SET and GO commands elicited natural triphasic commands, thereby substantiating the inherent capacity of the spinal network in generating them. Key points SummaryO_LISpinal sensorimotor circuits, despite extensive physiological analyses, remain poorly understood in the context of voluntary movement. C_LIO_LIThis study models the capabilities of these spinal networks, alongside musculoskeletal dynamics, to achieve single-joint arm flexion following minimum jerk principles. C_LIO_LIPreparatory (SET) and launch (GO) step commands modulate spinal network states, including neuron activity and synaptic strength. C_LIO_LINotably, arm movement results from sensorimotor interactions within spinal circuits, even with basic step commands that have no dynamics. C_LIO_LIA Goal Exploration Process (GEP), inspired by developmental baby babbling through trial and error, was used to refine step commands. C_LIO_LIThe spinal networks, when in appropriate states, were shown to spontaneously generate triphasic commands across a broad range of valid movement amplitudes and speeds. C_LIO_LIThese findings highlight the intrinsic capacity of spinal sensorimotor circuits to manage complex movement dynamics, offering novel testable insights as to their possible functional role in voluntary motor control. C_LI

neuroscience↗

bioRxiv2022

Activity-dependent decline and recovery of synaptic transmission in central parts of surviving primary afferents after their peripheral cut.

Whereas axons deprived of their nucleus degenerate within a few days in Mammals, they survive for several months in Crustacean. However, it is not known if central synapses from sensory axons may preserve their molecular machinery in the absence of spiking activity, after peripheral axotomy, which suppress their nucleus. Using electrophysiology techniques and electron microscopy imaging we report that 1) Electron microscopy analysis confirms previous observations that glial cell nucleus present in sensory nerve, proliferate an migrate to axon tubes, in which they form close contact with surviving axons; 2) after peripheral axotomy performed in vivo on Coxo-Basipodite chordotonal organ (CBCO) sensory nerve does not convey any sensory message, but antidromic volleys are observed; 3) Central synaptic transmission to motoneurons (MNs) progressively declines over #200 days (90% of monosynaptic excitatory transmission is lost after 3 weeks, whereas 60% of polysynaptic inhibitory transmission persist up to 6 months). After #200 days no transmission is observed anymore; 4) However, this total loss is only apparent, because repetitive electrical stimulation of the sensory nerve in vitro progressively restores first inhibitory post-synaptic potentials (IPSPs) then excitatory post-synaptic potentials (EPSPs); 5) The loss of synaptic transmission can be prevented by in vivo chronic sensory nerve stimulation; 6) Using simulations based on the geometric arrangements of synapses of the monosynaptic excitatory transmission and disynaptic inhibitory pathways, we have shown that antidromic activity in CBCO nerve could play a role in maintenance of synaptic function of inhibitory pathways to MNs, but not on monosynaptic excitatory transmission to MNs. Taken together, our study confirms the key role of glial nucleus in axon survival, that machinery for spike conduction and synaptic release even if no activity is present for several months. After long silence periods (>6 months) spike conduction and synaptic function can still be restored by electrical activity.

neuroscience↗

bioRxiv2021

A novel and specific regulator of neuronal V-ATPase in Drosophila

The V-ATPase is a highly conserved enzymatic complex that ensures appropriate levels of organelle acidification in virtually all eukaryotic cells. While the general mechanisms of this proton pump have been well studied, little is known about the specific regulations of neuronal V-ATPase. Here, we studied CG31030, a previously uncharacterized Drosophila protein predicted from its sequence homology to be part of the V-ATPase family. We found that this protein is essential and apparently specifically expressed in neurons, where it is addressed to synaptic terminals. We observed that CG31030 co-immunoprecipitated with V-ATPase subunits, in particular with ATP6AP2, and that synaptic vesicles of larval motoneurons were not properly acidified in CG31030 knockdown context. This defect was associated with a decrease in quantal size at the neuromuscular junction, severe locomotor impairments and shortened lifespan. Overall, our data provide evidence that CG31030 is a specific regulator of neuronal V-ATPase that is required for synaptic vesicle acidification and neurotransmitter release.

neuroscience↗