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Despite increasing representation in graduate training programs, a disproportionate number of women leave academic research without obtaining an independent position that enables them to train the next generation of academic researchers. To understand factors underlying this trend, we analyzed formal PhD and postdoctoral mentoring relationships in the life sciences during the years 2000 to 2020. Student and mentor gender are both associated with differences in rates of student’s continuation to positions that allow formal academic mentorship. Although trainees of women mentors are less likely to take on positions as academic mentors than trainees of men mentors, this effect is reduced substantially after controlling for several measurements of mentor status. Thus, the effect of mentor gender can be explained at least partially by gender disparities in social and financial resources available to mentors. Because trainees and mentors tend to be of the same gender, this association between mentor gender and academic continuation disproportionately impacts women trainees. On average, gender homophily in graduate training is unrelated to mentor status. A notable exception to this trend is the special case of scientists having been granted an outstanding distinction, evidenced by membership in the National Academy of Sciences, being a grantee of the Howard Hughes Medical Institute, or having been awarded the Nobel Prize. This group of mentors trains men graduate students at higher rates than their most successful colleagues. These results suggest that, in addition to other factors that limit career choices for women trainees, gender inequities in mentors’ access to resources and prestige contribute to women’s attrition from independent research positions.

As academic careers become more competitive, junior scientists need to understand the value that mentorship brings to their success in academia. Previous research has found that, unsurprisingly, successful mentors tend to train successful students. But what characteristics of this relationship predict success, and how? We analyzed an open-access database of 18,856 researchers who have undergone both graduate and postdoctoral training, compiled across several fields of biomedical science with an emphasis on neuroscience. Our results show that postdoctoral mentors were more instrumental to trainees’ success compared to graduate mentors. Trainees’ success in academia was also predicted by the degree of intellectual synthesis between their graduate and postdoctoral mentors. Researchers were more likely to succeed if they trained under mentors with disparate expertise and integrated that expertise into their own work. This pattern has held up over at least 40 years, despite fluctuations in the number of students and availability of independent research positions.

International audience; Glial cells have emerged as key players in the central control of energy balance and etiology of obesity. Astrocytes play a central role in neural communication via the release of gliotransmitters. Acyl-CoA binding protein (ACBP)-derived endozepines are secreted peptides that modulate the GABAA receptor. In the hypothalamus, ACBP is enriched in arcuate nucleus (ARC) astrocytes, ependymocytes and tanycytes. Central administration of the endozepine octadecaneuropeptide (ODN) reduces feeding and improves glucose tolerance, yet the contribution of endogenous ACBP in energy homeostasis is unknown. We demonstrated that ACBP deletion in GFAP+ astrocytes, but not in Nkx2.1-lineage neural cells, promoted diet-induced hyperphagia and obesity in both male and female mice, an effect prevented by viral rescue of ACBP in ARC astrocytes. ACBP-astrocytes were observed in apposition with proopiomelanocortin (POMC) neurons and ODN selectively activated POMC neurons through the ODN-GPCR but not GABAA, and supressed feeding while increasing carbohydrate utilization via the melanocortin system. Similarly, ACBP overexpression in ARC astrocytes reduced feeding and weight gain. Finally, the ODN-GPCR agonist decreased feeding and promoted weight loss in ob/ob mice. These findings uncover ACBP as an ARC gliopeptide playing a key role in energy balance control and exerting strong anorectic effects via the central melanocortin system.

Parkinson's disease is characterized by the death of dopaminergic neurons and the emergence of strong Beta-band oscillations throughout the basal ganglia nuclei. According to the mainstream theory, this synchrony is mediated by a dopamine deficit within the striatum creating a functional imbalance between the D1-expressing medium spiny neurons, which project to the internal segment of the globus pallidus, and D2-expressing one, which target its external segment, and ultimately leads to oscillatory activity. However, anatomical evidence gathered in rodents and primates has shown that striatal neurons are for the most part not organized into independent populations differentially targeting the two segments of the globus pallidus, nor alternatively expressing D1 or D2 receptors, thus calling for an alternative mechanism through which the lack of dopamine may cause oscillations. Here we adopt a computational approach in which we investigate a model whose parameters are fit to an extensive set of anatomical and physiological constraints from non-human primates, including axonal transmission delays gathered from eight experimental studies. Investigating the lack of dopamine in this model revealed that in the absence of segregated pathways, Beta-band oscillations emerge as a consequence of the extra-striate dopaminergic receptors reduced activity. These oscillations are caused by synchronous activity within the external globus pallidus-subthalamic nucleus loop, and their frequency are modulated by the transmission delays between these nuclei. Our model delivers a parsimonious explanation of oscillations that does not require any external driving influence from cortex, nor specific medium spiny neuron properties.

Introduction L’hypothalamus medio-basal (MBH) renferme des neurones gluco-excites impliques dans le controle de l’homeostasie glucidique. Neanmoins, les mecanismes mis en jeu dans la reponse au glucose de ces neurones sont inconnus mis a part des donnees preliminaires montrant l’implication d’especes actives de l’oxygene (EAOs). Certains canaux de la famille des « transient receptor potential-canonical ° » (TRPC), qui presentent une conductance ionique observee dans les neurones gluco-excites, sont directement modules par les EAOs. Nous avons emis l’hypothese qu’une voie de signalisation EAOs-TRPC-dependante est impliquee dans la reponse au glucose des neurones gluco-excites hypothalamiques. Materiels et methodes In vitro : l’activite de cellules dissociees de MBH de rats ou souris est enregistree par imagerie calcique en reponse a l’augmentation de la concentration en glucose de 2,5 a 10 mm, en presence d’inhibiteurs de canaux TRPC. In vivo: la secretion d’insuline induite par l’injection intra-carotidienne d’un bolus de glucose, la tolerance au glucose et a l’insuline sont etudiees en reponse a l’administration d’inhibiteurs TRPC dans le MBH chez le rat et chez des souris deficientes pour le canal TRPC3. Resultats L’intensite des reponses calciques au glucose des neurones gluco-excites diminue significativement en presence des inhibiteurs TRPC non selectifs ou TRPC3-selectifs. Ces donnees suggerent que ce canal est implique dans la reponse au glucose des neurones gluco-excites du MBH. In vivo, l’administration d’un inhibiteur TRPC3-selectif dans le MBH inhibe la secretion d’insuline induite par l’injection intracarotidienne de glucose. Les souris deficientes pour le canal TRPC3 presentent egalement un defaut de secretion d’insuline en reponse a cette injection, parallelement a une intolerance au glucose, une hyperglycemie a jeun et un surpoids. Conclusion Nos donnees mettent en evidence une nouvelle voie de signalisation EAOs-TRPC3 jouant un role clef dans la reponse au glucose des neurones gluco-excites de MBH et le controle de l’homeostasie glucidique. Declaration d’interet Les auteurs declarent ne pas avoir d’interet direct ou indirect (financier ou en nature) avec un organisme prive, industriel ou commercial en relation avec le sujet presente.

Removal of the adrenal glands, the main site for the synthesis of aldosterone, produces an intake of sodium that is essential for survival. Using central blockade of angiotensin II (Ang II) receptors with SarIle Ang II, previous studies have shown that this intake depends on the stimulation of the brain angiotensin system. In the present study, using intracerebroventricular injection of specific antagonists of Ang II type 1 (AT1) or type 2 (AT2) receptors (losartan and PD 123319, respectively), we confirm that activation of brain angiotensin is essential for the expression of adrenalectomy-induced NaCl intake. Moreover, we show that (a) AT1 but not AT2 receptor blockade alone suppresses NaCl intake and (b) doses of AT1 and AT2 receptor antagonists that separately have no effect on NaCl intake, suppress the behavior when combined. It is proposed that AT1 receptors mediate the natriorexigenic effect of Ang II and that AT2 receptors have a permissive role on AT1 receptor stimulation.

Introduction L'hypothalamus medio-basal (MBH) renferme des neurones specialises dits gluco-excites (neurones GE) capables de detecter des augmentations de la concentration en glucose. Nous venons de mettre en evidence in vitro que les canaux TRPC3 (transient receptor potential canonical type-3) sont necessaires a la reponse au glucose des neurones GE. L'objectif de cette etude est de determiner si, in vivo, ces canaux sont effectivement impliques dans la detection cerebrale du glucose et le controle de l'homeostasie energetique. Materiels et Methodes Le poids corporel, la prise alimentaire, la tolerance au glucose et la sensibilite a l'insuline ont ete mesures chez des souris deficientes pour le canal TRPC3 (souris TRPC3 KO) nourries avec un regime standard ou enrichi en gras (HFD) ou chez des souris dont le canal TRPC3 a ete selectivement delete dans le MBH (souris TRPC3MBH KO, obtenues par l'injection d'un adeno-associated virus exprimant la recombinase cre dans le MBH de souris TRPC3lox/lox). Resultats Les souris TRPC3 KO presentent une intolerance au glucose sans alteration de la secretion et de la sensibilite a l'insuline sous regime standard. L'intolerance au glucose de ces animaux est exacerbee sous regime HFD par rapport a des animaux sauvages. La stimulation vagale de la secretion d'insuline en reponse a une injection intracarotidienne de glucose (stimulation uniquement cerebrale) et la diminution de la prise alimentaire en reponse a l'injection intracerebroventriculaire de glucose sont alterees chez les souris TRPC3 KO. Enfin, les souris TRPC3MBH KO presentent une augmentation du poids corporel associee a une augmentation de la prise alimentaire sans modification significative de la tolerance au glucose six semaines apres l'injection des virus. Conclusions L'ensemble de ces donnees met en evidence le role clef des canaux TRPC3 du MBH dans la detection cerebrale du glucose et le controle de l'homeostasie energetique. Reste a determiner la part des canaux TRPC3 du MBH par rapport a ceux presents dans les tissus peri-pheriques (muscles) dans la regulation de l'homeostasie glucidique per se.

Rationnel Le controle de la balance energetique repose sur la detection de signaux metaboliques incluant les acides gras a longue chaine (AGLC) par l'hypothalamus medio-basal (HMB). Les AGLC agissent dans l'HMB pour inhiber la prise alimentaire et la production de glucose, cependant les voies metaboliques et types cellulaires impliques ne sont pas connus. Acyl-CoA Binding Protein (ACBP) est une proteine intracellulaire liant les AGLC-CoA et controlant leur metabolisme en peripherie. Dans le cerveau, ACBP est connu comme Diazepam Binding Inhibitor, un peptide secrete et clive en octadecaneuropeptide (ODN). L'administration centrale d'ODN exerce une action anxiogene et anorexigene. Cependant, le role d'ACBP endogene dans le metabolisme et effets centraux des AGLC ainsi que le controle de l'equilibre energetique reste inconnu. Materiels et methodes Par des approches complementaires in vitro, ex vivo et l'utilisation de modeles ACBP KO in vivo , nous avons teste si ACBP est implique dans le metabolisme et la detection hypothalamique des AGLC et le bilan energetique. Resultats 1- En immunohistochimie, ACBP est principalement exprime dans les astrocytes et tanycytes de l'HMB. 2- Le metabolisme intracellulaire de l'oleate mais pas du palmitate est altere dans les astrocytes et explants hypothalamiques de souris ACBP KO. 3- L'administration centrale d'ODN inhibe la prise alimentaire chez les souris sauvages mais pas chez les souris MC4R KO suggerant l'implication des neurones POMC. 4- Nos donnees d'electrophysiologie montrent qu'ODN active specifiquement les neurones anorexigenes POMC. 5- L'invalidation d'ACBP specifiquement dans les astrocytes via la strategie Cre-Lox n'affecte pas la balance energetique sous diete normale mais augmente la susceptibilite a developper l'obesite chez les souris femelles sous diete riche en graisses. Conclusion Ces resultats suggerent un double role d'ACBP comme regulateur du metabolisme des AGLC et gliotransmetteur implique dans le cross-talk entre astrocytes et neurones POMC et la regulation hypothalamique de l'equilibre energetique. Declaration d’interet Les auteurs declarent ne pas avoir d'interet direct ou indirect (financier ou en nature) avec un organisme prive, industriel ou commercial en relation avec le sujet presente.

Seizures starting in patients over 60 years old are frequent. Diagnosis is sometimes difficult and frequently under- or overrated. Cerebrovascular disorders are the main cause of a first seizure. Because of more frequent comorbidities, physiologic changes, and a higher sensitivity to drugs, treatment has some specificity in elderly people. The aim of this paper is to present the result of a consensus meeting held in October 2004 by a Belgian French-speaking group of epileptologists and to propose guidelines for the management and the treatment of epilepsy in elderly people.

Sodium (Na+) depletion induces sodium appetite to replenish Na+ loss. It appears to be a consequence of enhanced levels of aldosterone (Aldo) and angiotensin II (AII) in the plasma as well as in the brain. Mineralocorticoid pretreatment modifies the sensitivity of septo-preoptic neurons to locally applied AII and Aldo. Therefore, we investigated septo-preoptic neuronal sensitivities to AII and Aldo, as well as to the specific AII type-1 receptor (AT-1) non-peptide antagonist losartan (Los) and to the specific AII type-2 receptor (AT-2) non-peptide antagonist PD123319 after one Na+ depletion without repletion. We found that one Na+ depletion induced increases in the proportion of neurons inhibited by iontophoretic application of AII (20.5% vs. 7.8%, p=0.004) whereas, the proportion of neurons excited by Aldo was increased, (23.7% vs. 5%, p=0.001). Moreover, the proportion of neurons changing sensitivity to AII after one application of Aldo was increased in the furosemide group (44.2% vs. 20.4%, p=0.0123). The proportion of neurons inhibited by application of losartan was enhanced, (26.4% vs. 9.3%, p=0.03). No significant changes were found in response to PD123319 by itself. Moreover, there were more neurons which co-localized responses to both Los and PD123319 in the furosemide group than in the control group (29.7% vs. 8.6%, p=0.027). It is known that multidepletions induce an increased need-free sodium appetite and our present findings could well form part of the neuronal basis of this behavior.

A previous study has shown that DOCA pretreatment altered the responsiveness of neurons to microiontophoretic administration of angiotensin II (AII) and aldosterone (Aldo). This result coincided with an increase in activity in the septo-preoptic region and a decrease in activity of the central nucleus of the amygdala. The latter region is anatomically linked to the bed nucleus of the stria terminalis (BNST). Single unit activity was recorded in the BNST in response to iontophoretic application of AII, non-peptide AII-receptor antagonists or Aldo in DOCA-pretreated and in non-pretreated rats. DOCA-pretreatment significantly decreased the responsiveness to AII (28 cells (18.5%) vs. 8 cells (14.0%) u = 0.018 for excitation and 3 cells (8.6%) vs. 0 cells 0%, u = 0.011 for inhibition, P < 0.05) and to Aldo (24 cells (21.4%) vs. 4 cells (10.2%), u = 0.026 for excitation, and 3 cells (2.6%) vs. 0 cells, u = 0.009 for inhibition, P < 0.05) of the neurons localised in the BNST. A significant decrease was found in the inhibitory responses to iontophoretic application of losartan, an AII type-1 receptor (AT-1) antagonist (u = 0.042, P < 0.05). No significant differences were recorded with iontophoretic application of PD 123319, a specific AII-type-2 (AT-2) receptor antagonist. Therefore AT-1 receptors are likely responsible for the decreased responsiveness of the BNST correlated with the decrease in the activity within the amygdala.

International audience

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International audience; This text is an opportunity to make an initial assessment of the use of the microblogging platform Twitter at the French National Assembly. An analysis of the dates on which MPs' accounts were opened since 2008 shows a dynamic of appropriation structured into three main periods, each with its own specific logic of use. At the end of this process, in September 2012, at the opening of the fourteenth legislature, Twitter became an essential media space, which suggests the hypothesis of a reconfiguration of relations between MPs and journalists. In fact, Twitter appears to be an extension of the Four Columns Hall (the traditional place where MPs and journalists meet), online and therefore open and with a multiplied effect.; Ce texte est l'occasion de faire un premier point sur une réflexion concernant l'usage de la plateforme de micro blogging Twitter à l'Assemblée nationale française. L'analyse des dates d'ouverture des comptes des députés, depuis 2008, montre une dynamique d'appropriation structurée en trois périodes principales, auxquelles correspondent des logiques d'usages spécifiques. Au terme de ce processus, en septembre 2012, lors de l'ouverture de la quatorzième législature, Twitter constitue un espace médiatique incontournable, ce qui suggère l'hypothèse d'une reconfiguration des relations en députés et journalistes. De fait, Twitter paraît constituer une émanation de la salle des Quatre colonnes, en ligne, donc ouverte et à l'effet démultiplié.

International audience; L’article interroge des corpus de presse nationaux, réunionnais et mahorais à propos de la question des langues de Mayotte. Il révèle que – y compris à l’occasion du referendum du 29 mars 2009 sur la départementalisation – la situation sociolinguistique n’y est que très peu évoquée, et en tout cas en dehors des rubriques habituelles d’actualité. Si la presse, dans son ensemble, reprend des thèmes plutôt consensuels liés au débat public autour du referendum (droit des cadis, polygamie, état civil, politique migratoire, etc.), la situation du plurilinguisme mahorais n’est pratiquement pas soulevée, ou alors uniquement dans une optique de valorisation du français. L’hypothèse – vérifiée – est que le discours institutionnel apparaît très prégnant dans l’espace public médiatique : ce qui ne signifie pas, toutefois, qu’il ne peut guère évoluer.

International audience

International audience; This text is an opportunity to make an initial assessment of the use of the microblogging platform Twitter at the French National Assembly. An analysis of the dates on which MPs' accounts were opened since 2008 shows a dynamic of appropriation structured into three main periods, each with its own specific logic of use. At the end of this process, in September 2012, at the opening of the fourteenth legislature, Twitter became an essential media space, which suggests the hypothesis of a reconfiguration of relations between MPs and journalists. In fact, Twitter appears to be an extension of the Four Columns Hall (the traditional place where MPs and journalists meet), online and therefore open and with a multiplied effect.; Ce texte est l'occasion de faire un premier point sur une réflexion concernant l'usage de la plateforme de micro blogging Twitter à l'Assemblée nationale française. L'analyse des dates d'ouverture des comptes des députés, depuis 2008, montre une dynamique d'appropriation structurée en trois périodes principales, auxquelles correspondent des logiques d'usages spécifiques. Au terme de ce processus, en septembre 2012, lors de l'ouverture de la quatorzième législature, Twitter constitue un espace médiatique incontournable, ce qui suggère l'hypothèse d'une reconfiguration des relations en députés et journalistes. De fait, Twitter paraît constituer une émanation de la salle des Quatre colonnes, en ligne, donc ouverte et à l'effet démultiplié.