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Cabirol, M.-J.

Publications and source records attributed to Cabirol, M.-J..

3 recordsLinked to original sources

Functional maturation in abducens motoneurons populations during angular VOR larval development

Extraocular motoneurons are the final neuronal relay implicated in gaze motor control and are known to be subdivided in functional subgroups, differently implicated in ocular motion dynamics. However, the maturation of these functional populations of extraocular motoneurons, in relation with the development of gaze-stabilizing reflexes remains largely unexplored. In amphibian tadpoles, the angular vestibulo-ocular reflex (VOR) appears later than other visuo-vestibular ocular reflexes and matures until the metamorphosis climax. Two types of Abducens motoneurons have been described to participate to the angular VOR in larval frog: spontaneous motor units, exhibiting a robust resting activity and silent motor units recruited only during head motion. The aim of this study was to investigate the maturation of these two types of Abducens motor units in relation with the development of the angular VOR by evaluating their discharge dynamic in response to head rotation in semi-intact preparations of larval Xenopus laevis. During larval life, the discharge modulation during sinusoidal head rotations increases significantly for silent units only, demonstrating a better sensitivity of this Abducens motoneuron sub-population to horizontal semicircular canal activation. In addition, this functional maturation was accompanied by an increase of the myelination in the lateral rectus motor nerve, promoting a faster conductivity in late larval stages than in early one. These findings showed that the development of the angular VOR is supported by a selective maturation of extraocular motoneurons subpopulations, specifically implicated in the improvement of the ocular kinematic during the reflex.

neuroscience↗

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↗

Microglia shape the embryonic development of mammalian respiratory networks

Microglia, brain-resident macrophages, play key roles during prenatal development in defining neural circuitry function, including ensuring proper synaptic wiring and maintaining homeostasis. Mammalian breathing rhythmogenesis arises from interacting brainstem neural networks that are assembled during embryonic development, but the specific role of microglia in this process remains unknown. Here, we investigated the anatomical and functional consequences of respiratory circuit formation in the absence of microglia. We first established the normal distribution of microglia within the wild-type (WT, Pu.1+/+) mouse brainstem at embryonic ages when the respiratory networks are known to emerge (embryonic day (E) 14.5 for the parafacial respiratory group (epF) and E16.5 for the preBotzinger complex (preBotC)). In transgenic mice depleted of microglia (Pu.1-/- mutant), we performed anatomical staining, calcium imaging and electrophysiological recordings of neuronal activities in vitro to assess the status of these circuits at their respective times of functional emergence. Spontaneous respiratory-related activity recorded from reduced in vitro preparations showed an abnormally slow rhythm frequency expressed by the epF at E14.5, the preBotC at E16.5 and in the phrenic motor nerves from E16.5 onwards. These deficits were associated with a reduced number of active epF neurons, defects in commissural projections that couple the bilateral preBotC half-centers, and an accompanying decrease in their functional coordination. These abnormalities probably contribute to eventual neonatal death, since plethysmography revealed that E18.5 Pu.1-/- embryos are unable to sustain breathing activity ex utero. Our results thus point to a crucial contribution of microglia in the proper establishment of the central respiratory command during embryonic development.

neuroscience↗