News & Events

05/12/2018 10h00
Vladimir Ivosev, invited by Anna Beyeler
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Lieu: Neurocentre Magendie Seminar room

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PhD/HDR defense
30/11/2018 13h30
Laurie ROBIN - Roles of astroglial type 1 cannabinoid receptor (CB1) in memory and synaptic plasticity

- Roles of astroglial type 1 cannabinoid receptor (CB1) in memory and synaptic plasticity

The endocannabinoid system is an important modulator of physiological functions. It is composed of cannabinoid receptors, their endogenous lipid ligands (the endocannabinoids) and the enzymatic machinery for endocannabinoid synthesis and degradation. The type-1 cannabinoid receptors (CB1) are expressed in different cell types of the brain and are known to be involved in memory processes. Endocannabinoids are mobilized in an activity-dependent manner in brain areas involved in the modulation of memory such as the hippocampus. In this brain region, CB1 receptors are mainly expressed at neuronal pre-synaptic terminals where their stimulation inhibits the release of neurotransmitters, thereby modulating several forms of synaptic activity.
Besides their expression in neurons, CB1 receptors are also expressed in astrocytes. Along with the pre- and post-synaptic neurons, astrocytes are part of the “tripartite synapse”, where they participate in synaptic plasticity and associated memory processes. Interestingly, modulation of astroglial CB1 receptors has been proposed to facilitate glutamatergic transmission in the hippocampus. In this brain area, astrocytes regulate the activity of N-methyl-D-aspartate receptors (NMDARs) through the control of the synaptic levels of their co-agonist D-serine, thereby mediating long-term synaptic plasticity. However, the mechanisms inducing D-serine release by astrocytes are still not identified. Interestingly, our laboratory showed that the negative effect of exogenous cannabinoids on spatial working memory is mediated by astroglial CB1 receptors through a NMDAR-dependent mechanism in the hippocampus, but the physiological role of astroglial CB1 remains unknown.
One of the forms of memory involving CB1 receptors is novel object recognition memory (NOR). The exogenous stimulation of hippocampal CB1 receptors inhibits the consolidation of long-term NOR formation. Constitutive global deletion of CB1 receptors in mice leaves NOR intact, suggesting that endogenous CB1 receptor signaling is not necessary for long-term NOR. However, recent studies pointed-out that, likely due to compensatory mechanisms, the global deletion of the CB1 gene might mask cell typespecific roles of CB1 receptors, indicating that more sophisticated tools are required to fully understand the physiological roles of the endocannabinoid system in complex
behavioral functions.
In this work, we investigated the physiological role of the astroglial CB1 receptors on NOR formation and synaptic plasticity. By using a combination of genetic, behavioral, electrophysiological, imaging and biochemical techniques, we showed that endogenous activation of astroglial CB1 receptors is necessary for the consolidation of long-term NOR memory, through a mechanism involving the supply of D-serine to enhance synaptic NMDARs-dependent plasticity in the dorsal hippocampus. This study uncovers an unforeseen mechanism underlying D-serine release, triggering NMDARs activity and long-term memory formation.

Date de la soutenance: 30/11/2018 - 13h30
Lieu: module 2.1 (au dessus du RU)

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28/11/2018 10h00
Mehdi BHOURI from Montcouquiol-Sans's lab will give a presentation entitled 'Role of the planar cell polarity protein Vangl2 in hippocampal circuits involved in memory.'

28/11/2018 10h30
Marco MATOS from Oliet's lab will give a presentation entitled "Apolipoprotein E -ε4 in the development of synaptic impairment in Alzheimer's disease."

27/11/2018 11h00
Abel Eraso Pichot (Autonomous University of Barcelona)

Lieu: Neurocentre Magendie Seminar room

- Adaptive regulation of calcium excitability and energy metabolism by CREB-dependent transcription in astrocytes: study of the mechanisms governing astrocyte plasticity

An increasing body of evidence suggests that astrocytes participate in higher-brain functions, controlling from synaptic transmission to global brain waves and learning and memory processes. Different mechanisms have been proposed to mediate these astrocyte-dependent processes, astrocytic lactate release and calcium-dependent gliotransmission being the main known effectors. The existence of control of brain functions by astrocytes suggests that astrocytes may shape brain functions in response to experience as much as neurons, thus constituting the phenomenon of astrocyte plasticity. In neurons, the transcription factor CREB is the best known coordinator of synaptic and intrinsic plasticity. The fact that, in astrocytes, CREB activation is also activity-dependent, positions CREB as an ideal target to promote plasticity-related changes in astrocytes, too. In this study, we have analyzed the effect of the activation of CREB-dependent transcription in astrocytes, specifically regarding calcium signals and metabolism. We have demonstrated that activation of CREB-dependent transcription reduces cytosolic calcium events via mitochondria and increases lactate release, which may have impact on synaptic transmission. An important contribution of the study is the molecular analysis of astrocytic mitochondria, which has revealed that astrocytes may use fuels other than glucose such as fatty acids to meet basic energy metabolic demands. Taken together, our results establish astrocytic CREB as a hub in astrocyte-plasticity and shed light on the interplay between plasticity and energy metabolism in astrocytes.

PhD/HDR defense
26/11/2018 14h00
Thomas KERLOCH A study on the development of granular neurons of the dentate gyrus: morphogenesis and regulation by Rnd2.

A study on the development of granular neurons of the dentate gyrus: morphogenesis and regulation by Rnd2.
Date de la soutenance: 26/11/2018 - 14h00
Lieu: Neurocentre Magendie Seminar room

PhD/HDR defense
22/11/2018 14h30
Arjun A-BHASKARAN Cellular and circuit mechanisms of neocortical dysfunction in Fragile X Syndrome

Cellular and circuit mechanisms of neocortical dysfunction in Fragile X Syndrome
Date de la soutenance: 22/11/2018 - 14h30
Lieu: Magendie Salle de conference

General informations
Remittance of medals

Aude PANATIER receives her bronze medal from Nathalie Leresche (Charge de mission pour les Neurosciences, Institut des Sciences Biologiques du CNRS (INSB)) and Younis Hermés (Délégué Régional CNRS Aquitaine). more information here: the video dedicates to Aude

Collaboration Team Beyeler in Nature:
Dopamine modulates medial prefrontal cortex (mPFC) activity to mediate diverse behavioural functions. However, the precise circuit computations remain unknown. One potentially unifying model by which dopamine may underlie a diversity of functions is by modulating the signal-to-noise ratio in subpopulations of mPFC neurons. Here we demonstrate that dopamine increases the signal-to-noise ratio of responses to aversive stimuli in mPFC neurons projecting to the dorsal periaqueductal grey (dPAG). This data highlight how dopamine in the mPFC can selectively route sensory information to specific downstream circuits, representing a potential circuit mechanism for valence processing.

13/11/2018 14h00
Jean-Sébastien Jouhanneau

Lieu: CGFB - Salle de conférence

Synaptic mechanisms of sparse firing