Biology subjects

Vinit, S.

Publications and source records attributed to Vinit, S..

3 recordsLinked to original sources

bioRxiv2026

Cervical Repetitive Magnetic Stimulation Enhances Respiratory Recovery by Modulating Neuronal Plasticity After Cervical Spinal Cord Injury

Cervical spinal cord injury (SCI) frequently leads to life-threatening respiratory insufficiency by disrupting descending phrenic pathways. There is growing interest in non-invasive neuromodulatory approaches to enhance plasticity of spared respiratory circuits. We investigated whether cervical repetitive magnetic stimulation (rMS) applied to the injured cervical spinal cord promotes ventilatory recovery in a preclinical mouse model. Adult mice received a unilateral C3 hemicontusion followed by either rMS or sham stimulation. We found that rMS-treated mice significantly improved recovery of tidal volume and minute ventilation at 21 days post injury(dpi) compared to sham controls under various breathing conditions (isoflurane anesthesia, poikilocapnic phase and hypercapnic challenge). Correspondingly, diaphragm EMG enhanced ipsilateral hemidiaphragm activity in ventral and medial regions, and even contralateral hemidiaphragm activity in its ventral part. This was associated with a marked attenuation of the inflammatory response at the cervical spinal cord level. Indeed, rMS lowered astroglial, fibrotic scarring, pro-inflammatory CD68-, Iba1- microglial/macrophage markers. Moreover, perineuronal net expression (WFA positive staining) is globally reduced in the ventral spinal horn, whereas at the lesion site it is markedly increased and tightly wrapped around motoneurons. Together, these findings demonstrate that rMS promotes functional respiratory recovery after cervical SCI through combined enhancement of diaphragmatic motor output and modulation of the inflammatory and extracellular environment. Together, these functional and cellular findings indicate that spinal rMS promotes a permissive, pro-regenerative environment supporting respiratory circuit plasticity. We conclude that rMS significantly enhances ventilatory recovery via reduced inflammatory response and improved intraspinal rewiring after high cervical SCI, suggesting it is a promising non-invasive strategy. The ability of rMS to engage spared respiratory networks and support neuroplasticity highlights its promise as a safe, non-invasive therapeutic strategy with translational potential for rehabilitation of breathing function after SCI. One Sentence SummaryNoninvasive cervical magnetic stimulation improves breathing after spinal cord injury by boosting diaphragm activity and reducing inflammation.

neuroscience↗

bioRxiv2025

Unveiling Distinct Neuroimmune Responses in Mouse Models of Cervical Spinal Cord Injury: Hemisection versus Hemicontusion

Traumatic cervical spinal cord injury (cSCI) causes severe neurological deficits and long-term disability. Preclinical models such as cervical 2 (C2) hemisection (C2HS), resulting in disrupted communication between the respiratory centers and the phrenic motoneurons (PMN) pool, have been used since decades to study respiratory dysfunction and neuroinflammation after cSCI. Recently, contusive injuries such as C3 hemi-contusion (C3HC) have been increasingly used, as they induce phrenic motoneuron damage and offer a more clinically relevant model of SCI. However, these two different models may engage distinct pathophysiological cascades, raising concerns about the generalizability of findings across injury paradigms. In this study, we compared neuroimmune responses following C2HS or C3HC in mice. Animals underwent C2HS or C3HC, and spinal cord segments (C1-C8) were collected seven days post-injury for immuno-histological analyses around the lesion level and flow cytometry analyses at the lesion level. We observed that C2HS preserved more neurons and exhibited elevated CD86 and F4/80 expression. These markers are typically expressed by activated microglia and are indicative of a response oriented toward phagocytic and reparative functions. This phenotype was associated with limited pro-inflammatory cell infiltration and normalized level of systemic IL-6 in this model. Conversely, C3HC induced more extensive tissue damage, heightened microglial activation, a trend toward increased astrocytic reactivity, and significantly elevated CSPG levels on the contralateral side. Moreover, a persistent NK cell, neutrophil, and CD43 antigen-presenting cells infiltration, along with persistently high circulating IL-6 has been observed following C3HC. These findings demonstrate distinct neuroinflammatory signatures and repairing mechanisms between models, with C2HS promoting a microglia profile toward repair and C3HC leading to a prolonged and potentially harmful immune response. This study underscores, for the first time, how injury type shapes neuroimmune mechanisms, reinforcing the need for lesion-specific therapeutic strategies in cervical spinal cord injury. Highlight- C2 hemisection and C3 hemi-contusion trigger distinct neuroimmune responses in mice. - C2HS preserves ventral neurons and upregulates CD86 and F4/80, suggesting repair-oriented microglia. - C3HC induces CSPG accumulation, dendritic-like cell infiltration and prolonged systemic inflammation. - Injury model influences neuroimmune environment and regenerative potential after cervical SCI.

neuroscience↗

bioRxiv2024

Glycolytic metabolism modulation on spinal neuroinflammation and vital functions following cervical spinal cord injury

High spinal cord injuries (SCIs) often result in persistent diaphragm paralysis and respiratory dysfunction. Chronic neuroinflammation within the damaged spinal cord after injury plays a prominent role in limiting functional recovery by impeding neuroplasticity. In this study, we aimed to reduce glucose metabolism that supports neuroinflammatory processes in an acute preclinical model of C2 spinal cord lateral hemisection in rats. We administered 2-deoxy-D-glucose (2-DG; 200 mg/kg/day s.c., for 7 days) and evaluated the effect on respiratory function and chondroitin sulfate proteoglycans (CSPGs) production around spinal phrenic motoneurons. Contrary to our initial hypothesis, our 2-DG treatment did not have any effect on diaphragm activity and CSPGs production in injured rats, although slight increases in tidal volume were observed. Unexpectedly, it led to deleterious effects in uninjured (sham) animals, characterized by increased ventilation and CSPGs production. Ultimately, our results seem to indicate that this 2-DG treatment paradigm may create a neuroinflammatory state in healthy animals, without affecting the already established spinal inflammation in injured rats. Given the beneficial effects of 2-DG observed in other studies on neuronal activity and inflammation, adjusting 2-DG doses and/or increasing treatment duration should be explored to reduce deleterious inflammatory processes occurring after SCI.

physiology↗