Short Notes are concise reports which promote Open Science, by making accessible so far unshared scientific results. Find here the Short Notes accepted after review by experts. For detailed guidance or to share your research findings, visit the Short Notes submission platform.
Inès ACHIN, Céline PARIAS, Melody MORISSE, Baptiste MULOT, Olivier LASSERRE, Pascal CHEVREAU, Didier DUBREUIL, Emeline GALPIN, Thiery GASCOGNE, Karine LAROSE, Denis JEANTET, Regis PETIT, Cyril BLANCHET, Jean noel COUET, Pascal TONDEREAU, Gaëlle LEFORT, Scott LOVE, Elodie CHAILLOU
Posted on Tuesday September 16, 2025
DOI: 10.60675/vyhk-q978/sn20250916-4r/short-notes 
In sheep, the emotional valence of olfactory stimuli needs to be studied as olfaction is crucial for social and dietary preferences. To this end, it is necessary to evaluate the behavioural responses induced by olfactory stimuli (OS). These latter have often been explored with animals tested alone, in odorized versus non-odorized food choice tests or with constraining procedures. All these conditions are likely to induce emotional behaviours, which questions the specificity and reproducibility of behavioural responses induced by the OS. This study aimed to create an experimental setup for investigating the impact of OS on behavioural responses while addressing social and food resources and avoiding other confounding factors. Particularly, we focused on minimizing experimental bias through a habituation phase. To test our setup, we examined the consistency of behavioural responses measured in the control situation over time in adult ewes and lambs, by using principal component analysis. We found that the behavioural responses of individuals are similar over time and that the animals were not stressed by the experimental setup. Then, we concluded that it is adapted to explore the repulsive or attractive properties of the OS. Moreover, based on specific behaviours like vocalization, agitation, exploration, social contact, it could be possible to explore the emotional valence of OS.
Kassandra Kobon, David Pereira, Atef Asnacios , Pascal Maire, Voahangy Randrianarison-Huetz, Athanassia Sotiropoulos
Posted on Wednesday November 13, 2024
DOI: 10.60675/7gpx-md09/sn20241113-3r/short-notes
Repair of muscle tissue and growth of multinucleated myofibers depend on adult muscle stem cells (muSCs) and their ability to fuse. In this study, we took advantage of two genetic models of fusion-defective muSCs (both deleted for Serum response factor (Srf Mut), and one overexpressing alpha-actin (Srf Mut/Act+)) to decipher pathways and cellular properties that can restore fusion and gain insight into the mechanisms of mammalian muscle cell fusion. We first showed that Srf is involved in the fusion process after membrane mixing (hemifusion). Furthermore, Srf Mut and Srf Mut/Act+ muSCs were less rigid than control cells, and increasing apparent cell stiffness, presumably by increasing membrane and cortical tension, by hypotonic osmotic shock partially restored their fusion capacity, with a better efficacy when actin was overexpressed. These findings identify membrane and cortical tension/cell stiffness as a potential new player in myoblast fusion that may control Srf-dependent fusion in concert with the formation of actin structures at the fusion site.
Alexandre Faisant, Sandra Carignon, Arnaud Menuet, Nicolas Riteau, Marc Le Bert
Posted on Thursday February 29, 2024
DOI: 10.60675/b30k-ht75/sn001-2024/fc3r-short-notes
This study aimed to establish an experimental model of Guillain-Barré Syndrome (GBS), a peripheral inflammatory neuropathy in humans, using the Experimental Autoimmune Neuritis (EAN) model in C57BL/6 mice. This approach was informed by a comprehensive bibliographic analysis. While this experimental model has been developed successfully in rabbits, rats, and the SJL mouse strain, the literature on its application in C57BL/6 mice is limited. Our protocol analysis encompassed twenty-one articles utilizing the P0180-199 neurogenic peptide to induce EAN in this genetic background. Based on this literature, we selected one protocol for replication and made three adaptations. Despite using high-quality P0(180-199) peptide, we were unable to reproduce the selected EAN protocol or induce any pathological signs, even under optimized conditions. As a control to validate our reagents and methodology, we replicated a different model of inflammatory neuropathy targeting the central nervous system: the well-established Experimental Autoimmune Encephalitis (EAE) protocol. This replication was successful using the same C57BL/6 mouse genetic background and reagents, with the sole exception of the neurogenic peptide employed (MOG(35-55)).
