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BDM 2017 / 14-16 Mai

Le 22-23 Mai

Advanced Techniques for Synapse Biology

Bordeaux School of Neuroscience

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  • Séminaire - Lorenzo Cingolani

    28 avr. 2017 à 11:30 - Auditorium Bordeaux Neurocampus

    crucially depends on calcium channels...

    ► En savoir +
  • Pierre Philip et al. dans Scientific Reports

    3 avr. 2017

    un "psychiatre" bien accepté par les patients...

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  • K. Guillem & S. Ahmed dans Cerebral Cortex

    29 mars 2017

    un avantage sélectif pour gagner la compét...

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  • Emmanuel Mellet dans Frontiers in Human Neuroscience

    5 janv. 2017

    ..latéralité s’appuie sur une simulation motrice.

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  • M.Bourdenx, B. Dehay et al. dans Scientific Reports

    4 avr. 2017

    notre étude va à l’encontre de l’utilisation...

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Cocaine addiction as a homeostatic reinforcement learning disorder.Cocaine addiction as a homeostatic reinforcement learning disorder.
Drug addiction implicates both reward learning and homeostatic regulation mechanisms of the brain. This has stimulated 2 partially successful theoretical perspectives on addiction. Many important aspects of addiction, however, remain to be explained within a single, unified framework that integrates the 2 mechanisms. Building upon a recently developed homeostatic reinforcement learning theory, the authors focus on a key transition stage of addiction that is well modeled in animals, escalation of drug use, and propose a computational theory of cocaine addiction where cocaine reinforces behavior due to its rapid homeostatic corrective effect, whereas its chronic use induces slow and long-lasting changes in homeostatic setpoint. Simulations show that our new theory accounts for key behavioral and neurobiological features of addiction, most notably, escalation of cocaine use, drug-primed craving and relapse, individual differences underlying dose-response curves, and dopamine D2-receptor downregulation in addicts. The theory also generates unique predictions about cocaine self-administration behavior in rats that are confirmed by new experimental results. Viewing addiction as a homeostatic reinforcement learning disorder coherently explains many behavioral and neurobiological aspects of the transition to cocaine addiction, and suggests a new perspective toward understanding addiction.
Keramati M, Durand A, Girardeau P, Gutkin B, Ahmed SH.
Psychol Rev. 2017 Mar

Different CaV1.3 Channel Isoforms Control Distinct Components of the Synaptic Vesicle Cycle in Auditory Inner Hair Cells.Different CaV1.3 Channel Isoforms Control Distinct Components of the Synaptic Vesicle Cycle in Auditory Inner Hair Cells.
The mechanisms orchestrating transient and sustained exocytosis in auditory inner hair cells (IHCs) remain largely unknown. These exocytotic responses are believed to mobilize sequentially a readily releasable pool of vesicles (RRP) underneath the synaptic ribbons and a slowly releasable pool of vesicles (SRP) at farther distance from them. They are both governed by Cav1.3 channels and require otoferlin as Ca2+ sensor, but whether they use the same Cav1.3 isoforms is still unknown. Using whole-cell patch-clamp recordings in posthearing mice, we show that only a proportion (∼25%) of the total Ca2+ current in IHCs displaying fast inactivation and resistance to 20 μm nifedipine, a l-type Ca2+ channel blocker, is sufficient to trigger RRP but not SRP exocytosis. This Ca2+ current is likely conducted by short C-terminal isoforms of Cav1.3 channels, notably Cav1.342A and Cav1.343S, because their mRNA is highly expressed in wild-type IHCs but poorly expressed in Otof-/- IHCs, the latter having Ca2+ currents with considerably reduced inactivation. Nifedipine-resistant RRP exocytosis was poorly affected by 5 mm intracellular EGTA, suggesting that the Cav1.3 short isoforms are closely associated with the release site at the synaptic ribbons. Conversely, our results suggest that Cav1.3 long isoforms, which carry ∼75% of the total IHC Ca2+ current with slow inactivation and confer high sensitivity to nifedipine and to internal EGTA, are essentially involved in recruiting SRP vesicles. Intracellular Ca2+ imaging showed that Cav1.3 long isoforms support a deep intracellular diffusion of Ca2+SIGNIFICANCE STATEMENT Auditory inner hair cells (IHCs) encode sounds into nerve impulses through fast and indefatigable Ca2+-dependent exocytosis at their ribbon synapses. We show that this synaptic process involves long and short C-terminal isoforms of the Cav1.3 Ca2+ channel that differ in the kinetics of their Ca2+-dependent inactivation and their relative sensitivity to the l-type Ca2+ channel blocker nifedipine. The short C-terminal isoforms, having fast inactivation and low sensitivity to nifedipine, mainly control the fast fusion of the readily releasable pool (RRP); that is, they encode the phasic exocytotic component. The long isoforms, with slow inactivation and great sensitivity to nifedipine, mainly regulate the vesicular replenishment of the RRP; that is, the sustained or tonic exocytosis.
Vincent PF, Bouleau Y, Charpentier G, Emptoz A, Safieddine S, Petit C, Dulon D.
J Neurosci. 2017 Mar 15

NMDA-receptor-dependent plasticity in the bed nucleus of the stria terminalis triggers long-term anxiolysis.NMDA-receptor-dependent plasticity in the bed nucleus of the stria terminalis triggers long-term anxiolysis.
Anxiety is controlled by multiple neuronal circuits that share robust and reciprocal connections with the bed nucleus of the stria terminalis (BNST), a key structure controlling negative emotional states. However, it remains unknown how the BNST integrates diverse inputs to modulate anxiety. In this study, we evaluated the contribution of infralimbic cortex (ILCx) and ventral subiculum/CA1 (vSUB/CA1) inputs in regulating BNST activity at the single-cell level. Using trans-synaptic tracing from single-electroporated neurons and in vivo recordings, we show that vSUB/CA1 stimulation promotes opposite forms of in vivo plasticity at the single-cell level in the anteromedial part of the BNST (amBNST). We find that an NMDA-receptor-dependent homosynaptic long-term potentiation is instrumental for anxiolysis. These findings suggest that the vSUB/CA1-driven LTP in the amBNST is involved in eliciting an appropriate response to anxiogenic context and dysfunction of this compensatory mechanism may underlie pathologic anxiety states.
Glangetas C, Massi L, Fois GR, Jalabert M, Girard D, Diana M, Yonehara K, Roska B, Xu C, Lüthi A, Caille S, Georges F.
Nat Commun. 2017 Feb

Spatial and Temporal Regulation of Receptor Endocytosis in Neuronal Dendrites Revealed by Imaging of Single Vesicle Formation.Spatial and Temporal Regulation of Receptor Endocytosis in Neuronal Dendrites Revealed by Imaging of Single Vesicle Formation.
Endocytosis in neuronal dendrites is known to play a critical role in synaptic transmission and plasticity such as long-term depression (LTD). However, the inability to detect endocytosis directly in living neurons has hampered studies of its dynamics and regulation. Here, we visualized the formation of individual endocytic vesicles containing pHluorin-tagged receptors with high temporal resolution in the dendrites of cultured hippocampal neurons. We show that transferrin receptors (TfRs) are constitutively internalized at optically static clathrin-coated structures. These structures are slightly enriched near synapses that represent preferential sites for the endocytosis of postsynaptic AMPA-type receptors (AMPARs), but not for non-synaptic TfRs. Moreover, the frequency of AMPAR endocytosis events increases after the induction of NMDAR-dependent chemical LTD, but the activity of perisynaptic endocytic zones is not differentially regulated. We conclude that endocytosis is a highly dynamic and stereotyped process that internalizes receptors in precisely localized endocytic zones.
Rosendale M, Jullié D, Choquet D, Perrais D.
Cell Rep. 2017 Feb 21

The CB1 Receptor as the Cornerstone of Exostasis.The CB1 Receptor as the Cornerstone of Exostasis.
The type-1 cannabinoid receptor (CB1) is the main effector of the endocannabinoid system (ECS), which is involved in most brain and body functions. In this Perspective, we provide evidence indicating that CB1 receptor functions are key determinants of bodily coordinated exostatic processes. First, we will introduce the concepts of endostasis and exostasis as compensation or accumulation for immediate or future energy needs and discuss how exostasis has been necessary for the survival of species during evolution. Then, we will argue how different specific biological functions of the CB1 receptor in the body converge to provide physiological exostatic processes. Finally, we will introduce the concept of proactive evolution-induced diseases (PEIDs), which helps explain the seeming paradox that an evolutionary-selected physiological function can become the cause of epidemic pathological conditions, such as obesity. We propose here a possible unifying theory of CB1 receptor functions that can be tested by future experimental studies.
Piazza PV, Cota D, Marsicano G.
Neuron. 2017 Mar. Review


Opiacés : attention, danger mortel

25 avr. 2017

Aux USA entre 1999 et 2015, 183 000 personnes n’ont pas survécu à des surdoses d’opiacés prescrits. En quinze ans, les chiffres annuels ont été multip...► Lire la suite

La synapse électronique, premier pas vers un cerveau artificiel

4 avr. 2017

...La synapse artificielle mise au point par les chercheurs français constitue un premier pas vers le développement d'un « cerveau artificiel ». ► Lire la suite

Un “neurone géant” déterminant dans l'émergence de la conscience ?

30 mars 2017

...les chercheurs ont annoncé cette surprenante découverte. Ils émettent notamment l'hypothèse que cette cellule nerveuse d'un genre inédit chez un ma...► Lire la suite

L'AST: nous soutenons, valorisons et brevetons vos recherches...

6 mars 2017

...votre résultat de recherche pourra faire l’objet d’un dépôt d’une demande de brevet ou encore d’un programme de maturation soutenu financièrement p...► Lire la suite


Post-doc positions open 
A post-doctoral position is currently available
in the Institute of Cognitive and Integrative Neurosciences of Aquitaine in the team "Organization and Adaptability of Motor Systems", in Bordeaux..send their CV to Dr. Thoby-Brisson …

Recherchons ! Bordeaux Neurocampus: 
en ligne le 19 sept 2016 ....Recherchons: Chef de projet du centre  d’excellence sur  les maladies neurodégénératives CHU de Bordeaux Hôpital Pellegrin - Institut des Maladies Neurodégénératives

Recrutement PhD , ingénieurs , team leader etc...
SynDegen is currently able to offer 12 PhD student positions in the SynDegen ITN. Recrutons 2 thésards sur Bordeaux. Deadline pour les applications le 31 Janvier 2017…

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 Faculty of Health at Aarhus University, Call for applications........Proposition Poste MCU Poitiers : Le candidat travaillera dans l’équipe NeuroDéveloppement- NeuroAdaptation-NeuroDégénérescence au sein de l’UMR_S 1084 Inserm (LNEC)....



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