Un dispositif pour favoriser l’engagement des étudiants dans la rédaction de leur rapport de stage

Cet article rapporte la mise en place et l’analyse d’un dispositif qui a pour objectif de soutenir l’engagement des étudiants de master Métiers de l’édition dans l’écriture d’un rapport de stage. L’engagement sera étudié à travers le prisme de l’utilité, du sentiment d’efficacité personnelle et des attentes des étudiants (en termes de réussite). Le dispositif repose sur l’ajout i) d’un atelier sur l’identification et la formulation des compétences et ii) d’un rendu fractionné du rapport au dispositif existant (grille d’évaluation critériée et guide de rédaction). Les résultats suggèrent que l’atelier aide les étudiants à mieux appréhender les objectifs du rapport de stage et soutient leur engagement au travers d’une augmentation de la valeur attribuée à la tâche. Le feedback régulier via l’atelier et le rendu fractionné semblent renforcer le sentiment d’efficacité personnelle en améliorant la compréhension des objectifs du rapport de stage et de l’écriture réflexive. Le dispositif se veut également une ressource pour la suite de la carrière puisque les étudiants s’approprient des outils qui devraient favoriser leur insertion professionnelle

Fast non-genomic effects of progesterone-derived neurosteroids on nociceptive thresholds and pain symptoms

Abstract Fast Inhibitory controls mediated by glycine (GlyRs) and GABAA receptors (GABAARs) play an important role to prevent the apparition of pathological pain symptoms of allodynia and hyperalgesia. The use of positive allosteric modulators of these receptors, specifically expressed in the spinal cord, may represent an interesting strategy to limit or block pain expression. In this study, we have used stereoisomers of progesterone metabolites, acting only via non-genomic effects, in order to evaluate the contribution of GlyRs and GABAARs for the reduction of mechanical and thermal heat hypernociception. We show that 3a neurosteroids were particularly efficient to elevate nociceptive thresholds in naive animal. It also reduced mechanical allodynia and thermal heat hyperalgesia in the carrageenan model of inflammatory pain. This effect is likely to be mediated by GABAA receptors since 3b isomer was inefficient. More interestingly, 3a5b neurosteroid was only efficient on mechanical allodynia while having no effect on thermal heat hyperalgesia. We characterized these paradoxical effects of 3a5b neurosteroid using the strychnine and bicuculline models of allodynia. We clearly show that 3a5b neurosteroid exerts an antinociceptive effect via a positive allosteric modulation of GABAARs but, at the same time, is pronociceptive by reducing GlyR function. This illustrates the importance of the inhibitory amino acid receptor channels and their allosteric modulators in spinal pain processing. Moreover, our results indicate that neurosteroids, which are synthesized in the dorsal horn of the spinal cord and have limited side effects, may be of significant interest in order to treat pathological pain symptoms.

Antinociceptive action of oxytocin involves inhibition of potassium channel currents in lamina II neurons of the rat spinal cord

<p>Abstract</p> <p>Background</p> <p>Growing evidence in the literature shows that oxytocin (OT) has a strong spinal anti-nociceptive action. Oxytocinergic axons originating from a subpopulation of paraventricular hypothalamic neurons establish synaptic contacts with lamina II interneurons but little is known about the functional role of OT with respect to neuronal firing and excitability.</p> <p>Results</p> <p>Using the patch-clamp technique, we have recorded lamina II interneurons in acute transverse lumbar spinal cord slices of rats (15 to 30 days old) and analyzed the OT effects on action potential firing ability. In the current clamp mode, we found that bath application of a selective OT-receptor agonist (TGOT) reduced firing in the majority of lamina II interneurons exhibiting a bursting firing profile, but never in those exhibiting a single spike discharge upon depolarization. Interestingly, OT-induced reduction in spike frequency and increase of firing threshold were often observed, leading to a conversion of the firing profile from repetitive and delayed profiles into phasic ones and sometimes further into single spike profile. The observed effects following OT-receptor activation were completely abolished when the OT-receptor agonist was co-applied with a selective OT-receptor antagonist. In current and voltage clamp modes, we show that these changes in firing are strongly controlled by voltage-gated potassium currents. More precisely, transient I_Acurrents and delayed-rectifier currents were reduced in amplitude and transient I_Acurrent was predominantly inactivated after OT bath application.</p> <p>Conclusion</p> <p>This effect of OT on the firing profile of lamina II neurons is in good agreement with the antinociceptive and analgesic properties of OT described <it>in vivo</it>.</p

Unveiling the Impact of Morphine on Tamoxifen Metabolism in Mice in vivo

Background- Tamoxifen is used to treat breast cancer and cancer recurrences. After administration, tamoxifen is converted into two more potent antitumor compounds, 4OH-tamoxifen and endoxifen by the CYP3A4/5 and 2D6 enzymes in human. These active compounds are inactivated by the same UDP-glucuronosyltransferases isoforms as those involved in the metabolism of morphine. Importantly, cancer-associated pain can be treated with morphine, and the common metabolic pathway of morphine and tamoxifen suggests potential clinically relevant interactions. Methods- Mouse liver microsomes were used to determine the impact of morphine on 4OH-tamoxifen metabolism in vitro. For in vivo experiments, female mice were first injected with tamoxifen alone and then with tamoxifen and morphine. Blood was collected, and LC-MS/MS was used to quantify tamoxifen, 4OH-tamoxifen, N-desmethyltamoxifen, endoxifen, 4OH-tamoxifen-glucuronide and endoxifen-glucuronide. Results- In vitro, we found increased Km values for the production of 4OH-tamoxifen-glucuronide in the presence of morphine, suggesting an inhibitory effect on 4OH-tamoxifen glucuronidation. Conversely, in vivo morphine treatment decreased 4OH-tamoxifen levels in the blood while dramatically increasing the formation of inactive metabolites 4OH-tamoxifen-glucuronide and endoxifen-glucuronide. Conclusions- Our findings emphasize the need for caution when extrapolating results from in vitro metabolic assays to in vivo drug metabolism interactions. Importantly, morphine strongly impacts tamoxifen metabolism in mice. It suggests that tamoxifen efficiency could be reduced when both drugs are co-administered in a clinical setting, e.g. to relieve pain in breast cancer patients. Further studies are needed to assess the potential for tamoxifen-morphine metabolic interactions in humans

Spinal cellular and network properties modulate pain perception

Through the example the modulation of pain perception by a steroid hormone, I’m going to show you a multiscale interaction between two systems of an organism. Indeed, we will see how a the endocrine system via a molecule circulating in the blood will modulate its target molecule in the nervous system that will, in turn, change cellular activities at one stage of the central nervous system that could alter the behavior of this organism. Indeed our body collects somatosensory information from our environment that will be transmitted to the central nervous system by the peripheral nervous system. Amongst these sensory information there are nociceptive sensory inputs. A nociceptive stimuli detected at the level of the skin will be relayed by the spinal cord to the cortex where it will be interpreted as pain. The dorsal horn of the spinal cord is not a mere relay of the primary nociceptive input. At the level of the superficial layers of the dorsal horn, the nociceptive inputs are processed by a network of excitatory and inhibitory neurons before being transmitted via an ascending pathway to the brain where it will be interpreted as pain. At that level nociceptive processing is tuned by GABAA receptor-mediated inhibition in the spinal cord dorsal horn. These GABAergic inhibitory postsynaptic currents (IPSCs) are known to be modulated by spinally reduced steroids. Corticosterone (CORT) is a glucocorticoid produced by adrenal glands under the control of the hypothalamic-pituitary-adrenal axis. Circulating CORT can enter the central nervous system and be reduced to neuroactive reduced steroids, which modulate GABAA receptors. In the dorsal spinal cord, GABAergic transmission modulates integration of nociceptive information. It has been shown that enhancing spinal inhibitory transmission alleviates hyperalgesia and allodynia. Therefore, the spinal neuronal network is a pivotal target to counteract pain symptoms. Thus, any increase of spinal reduced steroids production enhancing GABAergic inhibition should reduce nociceptive messages integration and pain response. Previously, it has been shown that high levels of plasma glucocorticoids give rise to analgesia. However to our knowledge nothing has been reported regarding a direct non genomic modulation of neuronal spinal activity by peripheral CORT. In the present study, we used combined in vivo and in vitro electrophysiology approaches, associated with the measure of nociceptive mechanical sensitivity and plasma corticosterone level measurement to assess the impact of circulating CORT on rat nociception. We showed that CORT plasma level elevation produced analgesia via the reduction of nociceptive fiber mediated spinal responses. CORT is spinally reduced in the neuroactive metabolite THDOC that specifically enhances lamina II GABAergic synaptic transmission. The main consequence is a reduction of lamina II network excitability reflecting a selective decrease in processing of nociceptive inputs. The depressed neuronal activity at the spinal level then in turn leads to a weaker nociceptive message transmission to supraspinal structures and hence to an alleviation of pain

Spinal cellular and network properties modulate pain perception

Through the example the modulation of pain perception by a steroid hormone, I’m going to show you a multiscale interaction between two systems of an organism. Indeed, we will see how a the endocrine system via a molecule circulating in the blood will modulate its target molecule in the nervous system that will, in turn, change cellular activities at one stage of the central nervous system that could alter the behavior of this organism. Indeed our body collects somatosensory information from our environment that will be transmitted to the central nervous system by the peripheral nervous system. Amongst these sensory information there are nociceptive sensory inputs. A nociceptive stimuli detected at the level of the skin will be relayed by the spinal cord to the cortex where it will be interpreted as pain. The dorsal horn of the spinal cord is not a mere relay of the primary nociceptive input. At the level of the superficial layers of the dorsal horn, the nociceptive inputs are processed by a network of excitatory and inhibitory neurons before being transmitted via an ascending pathway to the brain where it will be interpreted as pain. At that level nociceptive processing is tuned by GABAA receptor-mediated inhibition in the spinal cord dorsal horn. These GABAergic inhibitory postsynaptic currents (IPSCs) are known to be modulated by spinally reduced steroids. Corticosterone (CORT) is a glucocorticoid produced by adrenal glands under the control of the hypothalamic-pituitary-adrenal axis. Circulating CORT can enter the central nervous system and be reduced to neuroactive reduced steroids, which modulate GABAA receptors. In the dorsal spinal cord, GABAergic transmission modulates integration of nociceptive information. It has been shown that enhancing spinal inhibitory transmission alleviates hyperalgesia and allodynia. Therefore, the spinal neuronal network is a pivotal target to counteract pain symptoms. Thus, any increase of spinal reduced steroids production enhancing GABAergic inhibition should reduce nociceptive messages integration and pain response. Previously, it has been shown that high levels of plasma glucocorticoids give rise to analgesia. However to our knowledge nothing has been reported regarding a direct non genomic modulation of neuronal spinal activity by peripheral CORT. In the present study, we used combined in vivo and in vitro electrophysiology approaches, associated with the measure of nociceptive mechanical sensitivity and plasma corticosterone level measurement to assess the impact of circulating CORT on rat nociception. We showed that CORT plasma level elevation produced analgesia via the reduction of nociceptive fiber mediated spinal responses. CORT is spinally reduced in the neuroactive metabolite THDOC that specifically enhances lamina II GABAergic synaptic transmission. The main consequence is a reduction of lamina II network excitability reflecting a selective decrease in processing of nociceptive inputs. The depressed neuronal activity at the spinal level then in turn leads to a weaker nociceptive message transmission to supraspinal structures and hence to an alleviation of pain

Le Diplôme Universitaire « Pédagogie dans l'Enseignement Supérieur » : un exemple de collapération

International audienceDans ce travail, nous proposons un retour d’expérience sur le dispositif pédagogique instauré dans le cadre du Diplôme Universitaire « Pédagogie de l’Enseignement Supérieur » porté par l’Institut de Développement et d’Innovation Pédagogique de l’Université de Strasbourg. Il s’agit d’une formation pour les enseignants dans laquelle ils sont amenés à mettre en place un projet pédagogique spécifique et d’évaluer les changements qu’il induit. Pour accompagner l'enseignant dans cette démarche, le DU était organisé autour de plusieurs moments clés : entretiens individuels, regroupements en promotion complète et ateliers de formation. Nous nous sommes donc demandés si ces moments favorisent plutôt l’apprentissage par la collaboration ou par la coopération. Pour répondre à cette question, nous avons soumis un questionnaire aux 13 participants au DU, 7 réponses ont été obtenues. A la lumière de ces dernières, il semble plus pertinent de représenter le moment d'apprentissage notamment comme un continuum entre coopération et collaboration. Les moments se répartissent en effet selon ces deux modalités, ce qui suggère in fine de considérer le dispositif pédagogique comme une méthode d’apprentissage “collapérative”