Biology subjects

Bertrand, S. S.

Publications and source records attributed to Bertrand, S. S..

3 recordsLinked to original sources

bioRxiv2024

When Little Means a Lot: Impact of a Brief Early-life Motor Training on Mouse Neuromuscular Development.

In this study, we aimed to determine the impact of an increase in motor activity during the highly plastic period of development of the motor spinal cord and hindlimb muscles in newborn mice. A swim training regimen, consisting of two sessions per day for two days, was conducted in 1 and 2-day-old (P1, P2) pups. P3-trained pups showed a faster acquisition of a four-limb swimming pattern, accompanied by dysregulated gene expression in the lateral motor column, alterations in the intrinsic membrane properties of motoneurons (MNs) and synaptic plasticity, as well as increased axonal myelination in motor regions of the spinal cord. Network-level changes were also observed, as synaptic events in MNs and spinal noradrenaline and serotonin contents were modified by training. At the muscular level, slight changes in neuromuscular junction morphology and myosin subtype expression in hindlimb muscles were observed in trained animals. Furthermore, the temporal sequence of acquiring the adult-like swimming pattern and postural development in trained pups showed differences persisting until almost the second postnatal week. A very short motor training performed just after birth is thus able to induce functional adaptation in the developing neuromuscular system that could persist several days. This highlights the vulnerability of the neuromuscular apparatus during development and the need to evaluate carefully the impact of any given sensorimotor procedure when considering its application to improve motor development or in rehabilitation strategies.

neuroscience↗

bioRxiv2024

Disruption of the CRF1 receptor eliminates morphine-induced sociability deficits and firing of oxytocinergic neurons in male mice

Substance-induced social behavior deficits dramatically worsen the clinical outcome of substance use disorders; yet, the underlying mechanisms remain poorly understood. Herein, we investigated the role for the corticotropin-releasing factor receptor 1 (CRF1) in the acute sociability deficits induced by morphine and the related activity of oxytocin (OXY)-and arginine-vasopressin (AVP)-expressing neurons of the paraventricular nucleus of the hypothalamus (PVN). For this purpose, we used both the CRF1 receptor-preferring antagonist compound antalarmin and the genetic mouse model of CRF1 receptor-deficiency. Antalarmin completely abolished sociability deficits induced by morphine in male, but not in female, C57BL/6J mice. Accordingly, genetic CRF1 receptor-deficiency eliminated morphine-induced sociability deficits in male mice. Ex vivo electrophysiology studies showed that antalarmin also eliminated morphine-induced firing of PVN neurons in male, but not in female, C57BL/6J mice. Likewise, genetic CRF1 receptor-deficiency reduced morphine-induced firing of PVN neurons in a CRF1 gene expression-dependent manner. The electrophysiology results consistently mirrored the behavioral results, indicating a link between morphine-induced PVN activity and sociability deficits. Interestingly, in male mice antalarmin abolished morphine-induced firing in neurons co-expressing OXY and AVP, but not in neurons expressing only AVP. In contrast, in female mice antalarmin did not affect morphine-induced firing of neurons co-expressing OXY and AVP or only OXY, indicating a selective sex-specific role for the CRF1 receptor in opiate-induced PVN OXY activity. The present findings demonstrate a major, sex-linked, role for the CRF1 receptor in sociability deficits and related brain alterations induced by morphine, suggesting new therapeutic strategy for opiate use disorders.

neuroscience↗

bioRxiv2022

A galanin-positive population of lumbar spinal cord neurons modulates sexual behavior and arousal

During sex, male arousal increases to the ejaculatory threshold, allowing genital sensory input to trigger ejaculation. While copulation and sexual arousal are thought to be centrally regulated by the brain, ejaculation is considered a reflex controlled by a spinal circuit. In this framework, the spinal cord is assumed to be strongly inhibited by descending input from the brain until the ejaculatory threshold, playing no role in the regulation of copulatory behavior. However, this remains untested. Here, we mapped the spinal circuit controlling the bulbospongiosus muscle, which is involved in sperm expulsion in mice. Our findings reveal that bulbospongiosus muscle-motor neurons receive input from galanin-expressing interneurons. This galanin-positive population receives genital input and, while its stimulation leads to bulbospongiosus muscle activity, the evoked muscle-potentials are dependent on spinalization, the males internal state and decrease with repeated stimulation. Moreover, ablation of galanin neurons affected the latency to ejaculate and altered the copulatory pattern. These results suggest an unexpected role of spinal circuits in the control of copulation and arousal, in addition to its established role in ejaculation.

neuroscience↗