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X-WR-CALNAME:Bordeaux Neurocampus
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X-WR-CALDESC:Events for Bordeaux Neurocampus
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DTSTART;TZID=Europe/Paris:20241212T100000
DTEND;TZID=Europe/Paris:20241212T100000
DTSTAMP:20260422T094519
CREATED:20241204T231433Z
LAST-MODIFIED:20241205T084259Z
UID:178394-1733997600-1733997600@www.bordeaux-neurocampus.fr
SUMMARY:Seminar - Elia Di Schiavi
DESCRIPTION:\n\n\n\n\nVenue: BBS \n \n\nDr Elia Di Schiavi\nInstitute of Biosciences and BioResources\, IBBR Naples\, Italy \n\n\n\n\n\nTitle\nIdentification of neuroprotective genes and drugs using a C. elegans model for Spinal Muscular Atrophy \nAbstract\nSpinal muscular atrophy (SMA) is a neurodegenerative disease caused by mutations in the survival motor neuron gene (Smn1). Smn1 is involved in mRNA splicing\, but motor neurons seem more sensitive to perturbations to Smn1. Why motor neurons are more affected to splicing alterations in SMA is still debated. Importantly\, in the last years three different drugs have been approved by FDA for SMA treatment\, nevertheless they resulted to be not efficacious for all the conditions or all types of SMA patients. So\, to 1) understand the specific role of Smn1 in mRNA splicing in motor neurons and 2) identify new potential therapeutic molecules to be used in combination with actual treatments\, we took advantage of a C. elegans SMA model that we developed. In this model smn-1\, the Smn1 ortholog\, is specifically silenced in motoneurons (MNs)\, causing an age-dependent neurodegeneration. Through the RNA-sequencing of induced pluripotent cell-derived motoneurons (iPSC-MNs) from SMA patients we identified differentially spliced genes\, enriched in RNA motif 7. This motif is specifically bound by SYNCRIP\, a spliceosomal component. We demonstrated that hrpr-1/SYNCRIP and smn-1 genetically interact in MNs in C.elegans and that they regulate the expression and the splicing pattern of ret-1/RTN in C. elegans\, in SMA mice and iPSC-MN. Then\, we successfully used the same model for an unbiased semi-automated drug screening of an FDA-approved library\, that allowed us to analyse 384 compounds/week in triplicate. By using this approach\, we identified several new exciting leading compounds counteracting smn-1 related neurodegeneration in C. elegans. Our results demonstrate that we are able to isolate genetic and pharmacological hits that specifically suppress MNs degeneration with an unbiased approach\, delivering major progresses in defining new treatments for preventing the neuronal death caused by Smn1/smn-1 loss in motoneurons.\n
URL:https://www.bordeaux-neurocampus.fr/en/event/seminar-elia-di-schiavi/
CATEGORIES:For scientists,home-event,Impromptu seminar
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DTSTART;TZID=Europe/Paris:20241212T140000
DTEND;TZID=Europe/Paris:20241212T140000
DTSTAMP:20260422T094519
CREATED:20241120T160733Z
LAST-MODIFIED:20241120T161611Z
UID:177772-1734012000-1734012000@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense - Rebecca Hekking
DESCRIPTION:Venue: Neurocentre Magendie – salle de conférence \nDefense in french \n\nRebecca Hekking\nOliet’s team\, Neurocentre Magendie \nSupervisor: Aude Panatier \nTitle\nIdentification of the role of astrocyte-derived extracellular vesicles in the regulation of synaptic transmission and synaptic plasticity\n \nAbstract\nBrain function relies on the transfer of information between neurons\, which occurs at a subcellular structure called the synapse. Interestingly\, the efficiency of a synapse can be modified under certain conditions\, potentiating or inhibiting information transfer. Over the past 20 years\, astrocytes\, a type of glial cells\, have been identified as key neuronal partners that are able to regulate synaptic transmission. Several pathways allowing astrocytes to regulate synaptic function have already been elucidated. Another interesting but under-investigated pathway would be through the release of extracellular vesicles. \nExtracellular vesicles (EVs) are small membrane-bound particles that contain bioactive molecules such as proteins\, nucleic acids\, and lipids. Most cells release these vesicles which allow them to exchange cellular components with neighbouring -but also sometimes distant- cells. Some studies suggest that astrocytes also release EVs\, yet it is still unclear whether these astrocyte-derived vesicles are involved in synaptic functions. \nThis thesis aims at elucidating whether astrocyte-derived extracellular vesicles play a key role in the regulation of synaptic transmission and plasticity. To address this question\, we have designed two complementary studies. \nWe first isolated astrocyte-derived EVs in vitro in order to investigate their release rate and their content. We have shown on one hand that exposing astrocyte cultures to ATP in vitro leads to an increase in the amount of small EVs released within 30 min of the stimulus. Furthermore\, the microRNA content of these vesicles is altered in response to the stimulus. A bioinformatics analysis predicted that the altered EV content could eventually affect signalling pathways involved in synaptic transmission in recipient cells. These changes seem to be induced specifically by ATP\, since exposure to the excitatory neurotransmitter glutamate or to the inhibitory neurotransmitter GABA did not modify the amount of small EVs released within 30 min of the stimulation. \nWe also studied the involvement of astrocyte-derived EVs in vivo. To this end\, we developed a virus that specifically targets astrocytes in the adult mouse brain and uses the Cas9 enzyme to invalidate a gene involved in EV biogenesis. Using this tool\, our preliminary data suggest that inhibiting the release of small EVs from astrocytes alters a form of synaptic plasticity in the hippocampus of adult male mice. \nTo conclude\, our findings suggest that small astrocyte-derived extracellular vesicles could indeed be involved in the regulation of some forms of synaptic plasticity and will hopefully encourage further studies to understand the underlying mechanisms. \nKey words : CRISPR-Cas9 system\, Electrophysiology\, Astrocyte\, Extracellular vesicle\, Long-term synaptic plasticity\, Synaptic transmission \nJury\n– Mme PANATIER\, Aude  – DR – Université de Bordeaux – Directrice de thèse\n– Mme ESCARTIN\, Carole – DR – Université Paris Saclay – Rapporteure\n– M. LEFEBVRE\, Christophe – PR – Université de Lille – Rapporteur\n– Mme MALNOU\, Cécile – PR – Université de Toulouse – Examinatrice\n– M. DELPECH\, Jean-Christophe – CR – Université de Bordeaux – Examinateur\n– M. FAVEREAUX\, Alexandre – DR – Université de Bordeaux  – Invité \n
URL:https://www.bordeaux-neurocampus.fr/en/event/thesis-defense-rebecca-hekking/
CATEGORIES:Thesis
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