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  • Symposium - 3° CONFÉRENCE BORDEAUX NEUROCAMPUS

    3 jours de débats, 20 conférenciers...

    ► En savoir +
  • Thomas Tourdias et al. dans Stroke

    29 juin 2016

    ...récupération motrice après un infarctus cérébra...

    ► En savoir +
  • Lucile Capuron, Julie Lasselin et al. dans Brain Behav Immun.

    20 juin 2016

    ...déficits de flexibilité cognitive chez le sujet...

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  • Cyril Herry: comment la peur nous fige ?

    16 juin 2016

    Neurocentre et Friedrich Miescher Institute...

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  • Séminaire - Scott Sternson

    8 juil. 2016 à 14:00 - Salle de conf Institut Magendie

    ..used to powerfully activate or inhibit neurons.

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PUBLICATIONS

Chronic stress does not further exacerbate the abnormal psychoneuroendocrine phenotype of Cbg-deficient male mice.Chronic stress does not further exacerbate the abnormal psychoneuroendocrine phenotype of Cbg-deficient male mice.
Chronic stress leads to a dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis which can constitute a base for pathophysiological consequences. Using mice totally deficient in Corticosteroid binding globulin (CBG), we have previously demonstrated the important role of CBG in eliciting an adequate response to an acute stressor. Here, we have studied its role in chronic stress situations. We have submitted Cbg ko and wild-type (WT) male mice to two different chronic stress paradigms - the unpredictable chronic mild stress and the social defeat. Then, their impact on neuroendocrine function - through corticosterone and CBG measurement - and behavioral responses - via anxiety and despair-like behavioral tests - was evaluated. Both chronic stress paradigms increased the display of despair-like behavior in WT mice, while that from Cbg ko mice - which was already high - was not aggravated. We have also found that control and defeated (stressed) Cbg ko mice show no difference in the social interaction test, while defeated WT mice reduce their interaction time when compared to unstressed WT mice. Interestingly, the same pattern was observed for corticosterone levels, where both chronic stress paradigms lowered the corticosterone levels of WT mice, while those from Cbg ko mice remained low and unaltered. Plasma CBG binding capacity remained unaltered in WT mice regardless of the stress paradigm. Through the use of the Cbg ko mice, which only differs genetically from WT mice by the absence of CBG, we demonstrated that CBG is crucial in modulating the effects of stress on plasma corticosterone levels and consequently on behavior. In conclusion, individuals with CBG deficiency, whether genetically or environmentally-induced, are vulnerable to acute stress but do not have their abnormal psychoneuroendocrine phenotype further affected by chronic stress.
de Medeiros GF, Minni AM, Helbling JC, Moisan MP.
Psychoneuroendocrinology. 2016 Apr 22;70:33-37

Development and localization of reverse-polarity mechanotransducer channels in cochlear hair cells.Development and localization of reverse-polarity mechanotransducer channels in cochlear hair cells.
Cochlear hair cells normally detect positive deflections of their hair bundles, rotating toward their tallest edge, which opens mechanotransducer (MT) channels by increased tension in interciliary tip links. After tip-link destruction, the normal polarity of MT current is replaced by a mechanically sensitive current evoked by negative bundle deflections. The "reverse-polarity" current was investigated in cochlear hair cells after tip-link destruction with BAPTA, in transmembrane channel-like protein isoforms 1/2 (Tmc1:Tmc2) double mutants, and during perinatal development. This current is a natural adjunct of embryonic development, present in all wild-type hair cells but declining after birth with emergence of the normal-polarity current. Evidence indicated the reverse-polarity current seen developmentally was a manifestation of the same ion channel as that evident under abnormal conditions in Tmc mutants or after tip-link destruction. In all cases, sinusoidal fluid-jet stimuli from different orientations suggested the underlying channels were opened not directly by deflections of the hair bundle but by deformation of the apical plasma membrane. Cell-attached patch recording on the hair-cell apical membrane revealed, after BAPTA treatment or during perinatal development, 90-pS stretch-activated cation channels that could be blocked by Ca2+ and by FM1-43. High-speed Ca2+ imaging, using swept-field confocal microscopy, showed the Ca2+ influx through the reverse-polarity channels was not localized to the hair bundle, but distributed across the apical plasma membrane. These reverse-polarity channels, which we propose to be renamed "unconventional" mechanically sensitive channels, have some properties similar to the normal MT channels, but the relationship between the two types is still not well defined.
Beurg M, Goldring AC, Ricci AJ, Fettiplace R.
Proc Natl Acad Sci USA. 2016 May 9

Early Fiber Number Ratio Is aSurrogate of Corticospinal Tract Integrity and Predicts Motor Recovery After Stroke.Early Fiber Number Ratio Is aSurrogate of Corticospinal Tract Integrity and Predicts Motor Recovery After Stroke.
BACKGROUND AND PURPOSE:
The contribution of imaging metrics to predict poststroke motor recovery needs to be clarified. We tested the added value of early diffusion tensor imaging (DTI) of the corticospinal tract toward predicting long-term motor recovery.
METHODS:
One hundred seventeen patients were prospectively assessed at 24 to 72 hours and 1 year after ischemic stroke with diffusion tensor imaging and motor scores (Fugl-Meyer). The initial fiber number ratio (iFNr) and final fiber number ratio were computed as the number of streamlines along the affected corticospinal tract normalized to the unaffected side and were compared with each other. The prediction of motor recovery (ΔFugl-Meyer) was first modeled using initial Fugl-Meyer and iFNr. Multivariate ordinal logistic regression models were also used to study the association of iFNr, initial Fugl-Meyer, age, and stroke volume with Fugl-Meyer at 1 year.
RESULTS:
The iFNr correlated with the final fiber number ratio at 1 year (r=0.70; P<0.0001). The initial Fugl-Meyer strongly predicted motor recovery (≈73% of initial impairment) for all patients except those with initial severe stroke (Fugl-Meyer<50). For these severe patients (n=26), initial Fugl-Meyer was not correlated with motor recovery (R(2)=0.13; p=ns), whereas iFNr showed strong correlation (R(2)=0.56; P<0.0001). In multivariate analysis, the iFNr was an independent predictor of motor outcome (β=2.601; 95% confidence interval=0.304-5.110; P=0.031), improving prediction compared with using only initial Fugl-Meyer, age, and stroke volume (P=0.026).
CONCLUSIONS: Early measurement of FNr at 24 to 72 hours poststroke is a surrogate marker of corticospinal tract integrity and provides independent prediction of motor outcome at 1 year especially for patients with severe initial impairment.
Bigourdan A, Munsch F, Coupé P, Guttmann CR, Sagnier S, Renou P, Debruxelles S, Poli M, Dousset V, Sibon I, Tourdias T.
Stroke. 2016 Apr;47(4):1053-9

MitoBrain, Putting energy into the brain.MitoBrain, Putting energy into the brain.
The brain is one of the most avid organs of the human body regarding energy consumption. Energy requirements of the brain are not only very high, but they also need to be very stable over time. Therefore, brain energy metabolism is tightly controlled by various metabolic pathways, among which mitochondria play a particularly relevant role. In addition, mitochondria are not only energy providers for the brain, but in the last decades a growing number of fascinating studies revealed that several of their functions play crucial roles in brain physiopathology.In this context, within the series of Bordeaux NeuroCampus Conferences, the first MitoBrain meeting was organized on October 1-3 2013 in Bordeaux (France) to bring together worldwide experts in different aspects of mitochondria and brain physiopathology. The aim of the meeting was to share different points of view and the newest progresses on the crucial question of the involvement of mitochondria in neurosciences. In this special issue of Neurobiology of Diseases, the organizing team of MitoBrain asked the participants to contribute review or original articles in order to emphasize some aspects and concepts, which were particularly debated during this meeting.Mitochondria, a double membrane organelle found in almost all eukaryotic cells, were first identified by Albert von Kölliker in 1857. In the late nineteenth century, they were described as “thread (in Greek; mitos) and granule (in Greek, chondros)”. Nowadays, mitochondria are viewed as a network that is structured by constant fusion and/or fission events. The articles from the groups of Pascale Belenguer and Pascal Reynier discuss the impact of mitochondria fusion/fission processes on physiological and pathological processes in the brain.From a spatial point of view, mitochondria move, which allow them exerting different functions at remote areas of cells. Mitochondrial mobility is particularly important for neurons considering that these cells have very polarized shapes, with extremely long axons and dendrites as compared to cell bodies. Therefore, mitochondrial mobility is finely regulated in neurons. One important aspect of this regulation is illustrated by the article by the group of Joseph Kittler, dealing with the role of calcium signaling on MIRO-dependent mitochondrial mobility.The subcellular organization of the mitochondrial network is also important as it shapes the functional interactions with other organelles. One of the best-characterized interactions is between mitochondria and endoplasmic reticulum, involving membrane domains with specific lipid and protein compositions, the MAM (Mitochondrial Associated Membrane). MAMs constitute true signaling crossroads, and the article by Giovanni Manfredi and Hibiki Kawamata reviews the physiological crosstalk between mitochondria and ER, and its disturbance in the pathology of amyotropic lateral sclerosis.
Mitochondrial mass is modulated during the lifespan of the cell, accordingly to the physiological state. This modulation involves mitochondrial biogenesis and degradation processes. Specific mitochondrial degradation by autophagy (also called mitophagy) is a recent finding that dramatically changed our view of mitochondrial turnover. Consistently, mitophagy is now subject of substantial investigations, which are particularly intense regarding neurodegenerative diseases, as testified by the review articles by the groups of Antony Shapira, Jorge Oliveira and Elena Ziviani.Albeit mitochondrial bioenergetic functions were deeply explored over the last century, their implications in brain functions are still poorly understood. Several questions remain unanswered regarding the role of mitochondria at a more integrative level. Especially, we still do not know what the direct consequences of mitochondrial metabolism remodeling are regarding (i) different brain cells, (ii) neuronal circuits and (iii) at behavior levels. Interestingly, by showing the regulation of spine synapse number by UCP2, the original article by Varela et al. (Tamas Horvath group) reveals clues on how mitochondrial bioenergetics might modulate neuronal activity under normal or hypoxic conditions.
Finally, the review article by Oliver Kann illustrates the role of mitochondrial energy metabolism in complex cortical information processing. This article highlights the high energy requirement of fast spiking inhibitory interneurons, a group of cells that play a key role in the emergence of fast network oscillations by synchronizing the activity of principal excitatory neurons. High-energy requirement implies high susceptibility to metabolic stress, and impairment of these interneurons might be involved in the pathophysiological mechanisms underlying several brain diseases such as Alzheimer’s disease, epilepsy and schizophrenia.
Thanks to the contribution from some of the key experts in the field, this Special Issue represents an interesting “state-of-the-art” of what is known concerning certain important mechanisms linking bioenergetics, mitochondria and brain functions. Of course, much is still to be clarified. For instance, the brain is for sure the most heterogeneous organ of the body. Despite a continuous and laborious work of classification, new types of neurons or glial cells are discovered almost on a daily base. Properties and functions of mitochondria are likely different, depending on the cells and the subcellular compartments where they are contained and the functional status of networks. Future work will have to deeply investigate the cellular, subcellular and functional specificities of mitochondria in the brain. Behavior is obviously the main function regulated by the brain. Very little is known so far on the impact of mitochondrial activity on behavioral processes. New studies appeared in the last years attempting to establish this link, and many more are awaited in the next future. Finally, the study of subcellular organelles in a complex and heterogeneous organ such as the brain is a difficult challenge. New technological and experimental approaches will have to be developed in the future, such as the possibility to manipulate single organelles in specific cells or to visualize mitochondrial behavior during ongoing brain functioning.
In summary, we believe that the relationship between mitochondrial functions and brain processes is one of the most fascinating challenges of neuroscience. It requires the merging of different expertises and the open discussion among scientists with different backgrounds. We are convinced that the meeting MitoBrain and the present Special Issue are strong examples of these interactions and we hope that they can contribute establishing the bases for a continuous growth of this exciting field of science.
Benard G, Bezard E, Marsicano G, Pouvreau S. Neurobiol Dis. 2016 Jun;90:1-2

Serotonergic modulation of the activity of mesencephalic dopaminergic systems: Therapeutic implications.Serotonergic modulation of the activity of mesencephalic dopaminergic systems: Therapeutic implications.
Since their discovery in the mammalian brain, it has been apparent that serotonin (5-HT) and dopamine (DA) interactions play a key role in normal and abnormal behavior. Therefore, disclosure of this interaction could reveal important insights into the pathogenesis of various neuropsychiatric diseases including schizophrenia, depression and drug addiction or neurological conditions such as Parkinson's disease and Tourette's syndrome. Unfortunately, this interaction remains difficult to study for many reasons, including the rich and widespread innervations of 5-HT and DA in the brain, the plethora of 5-HT receptors and the release of co-transmitters by 5-HT and DA neurons. The purpose of this review is to present electrophysiological and biochemical data showing that endogenous 5-HT and pharmacological 5-HT ligands modify the mesencephalic DA systems' activity. 5-HT receptors may control DA neuron activity in a state-dependent and region-dependent manner. 5-HT controls the activity of DA neurons in a phasic and excitatory manner, except for the control exerted by 5-HT2C receptors which appears to also be tonically and/or constitutively inhibitory. The functional interaction between the two monoamines will also be discussed in view of the mechanism of action of antidepressants, antipsychotics, anti-Parkinsonians and drugs of abuse.
De Deurwaerdère P, Di Giovanni G.
Prog Neurobiol. 2016 Mar 22. pii: S0301-0082(15)30096-4. Review.

The Cortical Processing of Sensorimotor Sequences is Disrupted in Writer's Cramp.The Cortical Processing of Sensorimotor Sequences is Disrupted in Writer's Cramp.
Evidence for pre-existing abnormalities in the sensory and motor systems has been previously reported in writer's cramp (WC). However, the processing of somatosensory information during motor planning has received little attention. We hypothesized that sensorimotor integration processes might be impaired partly due to a disruption in the parieto-premotor network. To test this assumption, we designed 2 nonwriting motor tasks in which subjects had to perform a 4-finger motor sequence either on the basis of sensory stimuli previously memorized (SM task) or freely generated (SG task). Brain activity was measured by combining event-related functional magnetic resonance imaging and coherency electroencephalography in 15 WC patients and 15 normal controls. The bold signal was decreased in patients in both tasks during sensory stimulation but not during movement execution. However, the EEG study showed that coherency was decreased in patients compared with controls, during the delay of the SM task and during the execution of the SG task, on both the whole network and for specific couples of electrodes. Overall, these results demonstrate an endophenotypic impairment in the synchronization of cortical areas within the parieto-premotor network during somatosensory processing and motor planning in WC patients
Langbour N, Michel V, Dilharreguy B, Guehl D, Allard M, Burbaud P.
Cereb Cortex. 2016 Apr 24.

Brèves...

USA: 1er accident mortel d'une voiture Tesla

1 juil. 2016

C'est le premier accident mortel sur les quelque 200 millions de kilomètres parcourus par des véhicules équipés d'Autopilot, affirme Tesla....► Lire la suite

Shock, sadness, anger: Here's what scientists are tweeting about #Brexit

27 juin 2016

about #Brexit.....Researchers deplore U.K. decision to leave the European Union....► Lire la suite

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Recherchons ! Recrutement d’un Ingénieur d’Etude « en Biologie Moléculaire et Cellulaire » INSERM . L’équipe « Polarité Planaire et Plasticité » qui vient d’être labélisée Equipe FRM 2016 recrute un ingénieur d’étude en CDD, responsable de son activité de biologie...
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