Biology subjects

Soubeyre, V.

Publications and source records attributed to Soubeyre, V..

4 recordsLinked to original sources

bioRxiv2026

Oxytocin Modulation of Spinal Circuits Drives Therapeutic Benefits of Massage

Across social species, social touch enhances well-being and reduces pain -- two seemingly distinct benefits that enhance survival. Yet where and how the nervous system integrates these functions, and whether a single mechanism could serve both, remains unknown. Here we show that massage triggers oxytocin release, which shapes both pain and touch reward at the earliest stage of central processing -- the spinal cord -- through a single, state-dependent circuit mechanism. We report that in humans, massage enhances well-being, effects that correlate with endogenous oxytocin release. In mice, gentle touch activates hypothalamic oxytocin neurons that project directly to the spinal dorsal horn. Genetic manipulation of spinal oxytocin circuits alters behavioral responses to both gentle touch and noxious stimuli. Spinal calcium imaging and slice electrophysiology reveal that oxytocin acts on both excitatory and inhibitory spinal neurons to sculpt the relative activity of spinal ascending systems that convey both social touch and pain to the brain. Extending these findings to humans, we show that oxytocin receptors are also expressed on spinal excitatory and inhibitory neurons, and that endogenous oxytocin during massage correlates with altered spinal touch processing. Thus, spinal oxytocin signaling provides an evolutionarily conserved mechanism for the therapeutic benefits of massage.

neuroscience↗

bioRxiv2025

Western diet reversibly alters the olfactory mucosa and impairs the response to appetitive food cues

Current feeding behaviors contribute to the epidemic levels of obesity and diabetes observed in Europe and worldwide. Together with other sensory modalities, olfaction is involved in the control of food intake. Olfactory cues can influence eating behaviors, yet the nutritional status and diet can also alter olfactory abilities. Patients with metabolic disorders present impaired olfactory sensitivity which could in turn worsen their eating behaviors. Here we examined the short-term impact of a Western diet enriched in fat and sugar (High-Fat High-Sugar, HFHS) on the anatomy and physiology of the olfactory epithelium of mice. After 8 weeks of diet, HFHS fed animals presented higher adiposity without overweight, were glucose intolerant without any change in basal blood glucose or plasma insulin. A buried food test indicated impaired olfactory capacities in the HFHS group. Whereas food related odours increased food intake in control chow fed animals, HFHS mice showed an altered response to olfactory appetitive food cues. HFHS fed mice presented olfactory sensory neurons (OSN) with shorter cilia. Finally, electro-olfactogram (EOG) recorded in response to different odorant molecules showed lower amplitudes in HFHS fed mice. HFHS diet withdrawal during one month at the end of the HFHS diet exposure improved metabolic parameters and restored both the OSN cilia length and EOGs. Our results show that diet enriched in fat and sugar can rapidly alter the physiology of the olfactory epithelium before the development of significant metabolic disorders. Anatomical changes of individual olfactory sensory neurons may participate to the reduced olfactory sensitivity.

neuroscience↗

bioRxiv2024

Primary sensory neuron dysfunction underlying mechanical itch hypersensitivity in a Shank3 mouse model of autism

Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder marked by social deficits, repetitive behaviors, and atypical sensory perception. The link between ASD and skin abnormalities, inducing itchiness, has never been investigated in depth. This study explores mechanical itch sensitivity in the Shank3{Delta}C/{Delta}C mouse model. Key observations include heightened scratching in response to skin deformation and hypersensitivity to mechanical itch (i.e. alloknesis) in Shank3{Delta}C/{Delta}C mice. In Shank3{Delta}C/{Delta}C mice, ex vivo electrophysiological experiments revealed that C-fiber low-threshold mechanoreceptors (C-LTMRs) were hyporesponsive, and transcriptomic analysis showed a downregulation of TAFA4, a protein secreted by C-LMTRs. Interestingly, pharmacologically inhibiting A{beta}-LTMR, important in mechanical itch initiation, abolished the itch hypersensitivity. Also, TAFA4 injections reduced the spontaneous scratching response to skin deformation but failed to restore itch sensitivity. Our data suggest that somatosensory deficits in Shank3{Delta}C/{Delta}C mice lead to hypersensitivity to itchiness and indicate that two pathways might regulate mechanical itchiness, dependent on TAFA4.

neuroscience↗

bioRxiv2023

Induction of antiviral Interferon-Stimulated Genes (ISGs) by neuronal STING promotes the resolution of pain

Inflammation and pain are intertwined responses to injury, infection, or chronic diseases. While acute inflammation is essential in determining pain resolution and opioid analgesia, maladaptive processes occurring during resolution can lead to the transition to chronic pain. Here we found that inflammation activates the cytosolic DNA-sensing protein Stimulator of Interferon Genes (STING) in DRG nociceptors. Neuronal activation of STING promotes signaling through TANK-binding kinase 1 (TBK1) and triggers an interferon-beta (IFN{beta}) response that mediates pain resolution. Notably, we found that mice expressing a nociceptor-specific gain-of-function mutation in STING exhibited an IFN gene signature that reduced nociceptor excitability and inflammatory hyperalgesia through a KChIP1-Kv4.3 regulation. Our findings reveal a role of IFN-regulated genes (IRGs) and KChIP1 downstream of STING, in the resolution of inflammatory pain.

neuroscience↗