Neurocentre Magendie

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29/05/2019 10h30
Anes JU from Beyeler's lab will give a presentation entitled "Serotonin receptor expression of the insular cortex involved in anxiety"

03/05/2019 14h00
Dr. Julia Lemos, Dissecting the actions of CRF in the NAc

Meeting room: Amphi Centre Broca

Dr. Julia Lemos is an Assistant Professor at the Department of Neuroscience of the University of Minnesota (USA) and will present the work of her lab dissecting the actions of corticotropin releasing factor (CRF) in the nucleus accumbens.
Host: Anna Beyeler

Outside of its well-characterized actions in the HPA axis, the stress-associated peptide corticotropin-releasing factor (CRF) regulates neuronal excitability and synaptic transmission in several extrahypothalamic brain regions. Previous research has shown that CRF in the nucleus accumbens (NAc) promotes appetitive behavior through mechanisms that remain poorly understood. We have recently showed that CRF potentiates both dopaminergic and cholinergic transmission in the NAc. However, it is unknown how CRF regulates the activity of medium spiny neurons (MSNs), the principle projection neurons of the NAc, to modulate behavioral output. MSNs are classified by their peptide expression and projection targets within the basal ganglia: dMSNs form the direct projection pathway and express dynorphin, whereas iMSNs form the indirect pathway and express enkephalin. RNAscope in situ hybridization was used to assess Crh1 mRNA expression in MSN subpopulations, identifying dMSNs and iMSNs with expression of dynorphin (pdyn) or enkephalin (pEnk), respectively. 20% of all cells were positive for Crh1 mRNA, with approximately 30% co-expressing pEnk mRNA (iMSNs), 30% co-expressing pDyn mRNA (dMSNs) and 30% co-expressing neither marker. Using whole-cell patch clamp electrophysiology recordings in brain slices, we examined the function of exogenously-applied CRF on the excitability of MSNs in the NAc core. Application of 100 nM CRF produced a leftward shift in the current-voltage relationship, demonstrating that CRF can enhance the firing rate of both dMSNs and iMSNs. Next steps will focus on identifying the role of CRF receptor subtypes in enhancing the spiking activity in MSNs and elucidate whether this effect is through direct actions on MSNs or through dopaminergic and cholinergic modulation of MSNs.

19/12/2018 10h30
Sebastien DELCASSO from Beyeler's lab will give a presentation entitled "Anatomical and functional organization of valence circuits in the insular cortex."

05/12/2018 10h00
Vladimir Ivosev, invited by Anna Beyeler

Meeting room: Neurocentre Magendie Seminar room

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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.

21/09/2018 11h30
Jason Shepherd, University of Utah - Host Anna Beyeler

Meeting room: Amphithéâtre du Centre Broca Nouvelle-Aquitaine

Inter-cellular RNA transfer: a novel role of the neuronal gene Arc which encodes a repurposed retrotransposon protein

The neuronal gene Arc is essential for long-lasting information storage in the mammalian brain. We recently found that Arc self-assembles into virus-like capsids that encapsulate RNA. Endogenous Arc protein is released from neurons in extracellular vesicles that mediate the transfer of Arc mRNA into new target cells. These results show that Arc exhibits similar molecular properties to retroviral Gag proteins. Evolutionary analysis indicates that Arc is derived from a vertebrate lineage of Ty3/gypsy retrotransposons, which are also ancestors to retroviruses. These findings suggest that Gag retroelements have been repurposed during evolution to mediate intercellular communication in the nervous system. Our working model posits that Arc protein is locally translated in dendrites, where it forms a capsid that binds local mRNAs that are transported out of the cell.

15/06/2018 11h30
François Amaury

Meeting room: Amphi Broca Nouvelle-Aquitaine

from Institut de génomique fonctionnelle de Montpellier, Department of Neuroscience's lab will give a presentation entitled 'RVM GABAergic neurons command enkephalinergic spinal neurons to act as gatekeepers of mechanical pain.'

Invitant : Pascal Fossat , Assistant Professor, Team: Central Mechanisms of Pain Sensitization and Anna Beyeler: Teamleader 'Neural Circuits of Anxiety', IINS et Neurocentre Magendie

17/05/2018 09h00
Neurocampus day

Meeting room: Université, Agora du Haut Carré, Talenc

Point fort de l’année ! le « Neurocampus Day » avec ses 6 instituts de recherche, ses rencontres, ses échanges prometteurs , une journée riche en sciences du cerveau... Domaine du Haut Carré , Talence le Jeudi 17 Mai 2018

Du Neurocentre Magendie:
14h40-15h05 Anna Beyeler / Anatomical and functional organization of neural populations in the amygdala and insula

17h15-17h40 Luigi Bellochio (Equipe Marsicano) / Striatonigral mitochondrial CB1 receptors mediate cannabinoid-induced catalepsy

10/04/2018 10h00
Davide Amato

Meeting room: Neurocentre Magendie Seminar room

Davide Amato will present his latest work on the role of D1 and D2 neurons of the nucleus accumbens in cocaine sensitization and cross-sensitization with antipsychotics. The study he will share was performed with single-cell calcium imaging in freely moving mice.

Invited by Anna Beyeler.

The team of Ian Wickersham at MIT developped a new generation of non toxic rabies vectors. Anna Beyeler was part of the team showing that neurons were still functioning normally up to four months after infection. In this new construct the gene coding for the polymerase necessary for transcribing viral genes was deleted. Without this gene, the virus becomes less harmful and infected cells can survive much longer.