Добірка наукової літератури з теми "Epine dendritiques"
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Дисертації з теми "Epine dendritiques":
Breton, Victor. "Elucider le rôle de VAMP7 dans les remodelages membranaires au cours des phénomènes d'apprentissages et de la mémoire." Electronic Thesis or Diss., Université Paris Cité, 2023. http://www.theses.fr/2023UNIP7048.
To transmit information from one neuron to another, neuronal cells use specialized communicating junctions called synapses. In the hippocampus, a large proportion of excitatory synapses are located in tiny membrane protrusions called dendritic spines. The dynamics and morphology of the spines change over time, depending on the activity to which the synapse is subjected. The pre- and post-synaptic zones are subject to a dense and active intracellular traffic. Among the proteins that regulate this traffic, we can find SNAREs (Soluble N-ethylmaleimide-sensitive-factor Attachment protein REceptor) which are mediating membrane fusion. This process allows vesicles to fuse with targeted membrane and enable the release of: neurotransmitters (pre-synaptic) or synaptic receptors (post-synaptic). SNARE proteins are classified into two main categories: v-SNAREs, found on the vesicle membrane, and t-SNAREs, found on targeted membrane. v- and t-SNAREs interact with each other to bring the two membranes together and trigger membrane fusion. The aim of my thesis was to determinate the role of intracellular trafficking in the membrane remodeling during learning and memory. My work focused on the v-SNARE VAMP7, which is expressed in neurons from developmental to mature stages, although little is known about its role in dendrites. Previously in the laboratory, it has been shown that VAMP7 KO mice show improved memory performance in behavioral tests involving learning and memory. First, I showed that VAMP7 is localized preferentially in dendrites. Then, I quantified on electron microscopy that VAMP7 KO mice show an increase in mature dendritic spines, confirming a role for VAMP7 in learning and memory processes. Using microscopy, I showed that VAMP7 is localized in close proximity to synapses and that VAMP7 is found in a large majority of dendritic spines, particularly in the head of these. To determinate its function, I assessed the distribution of VAMP7 and classical intracellular compartments (early and recycling endosomes, endolysosomes, etc.) in dendrites. My results indicate that VAMP7 is not predominantly localized in these compartments, suggesting the existence of an uncharacterized dendritic compartment. Using live imaging and super-resolution imaging, STED and STORM, I show that VAMP7 is localized in dendritic golgi extensions (Golgi sattelite). Finally, my results show that VAMP7 and some type of NMDA receptors are in the same compartments in both dendritic shaft and spines. In addition to studying the role of VAMP7 in membrane remodeling processes, I have, in collaboration with chemists specializing in the synthesis of fluorescent probes, discovered and developed the use of photoconvertible organic probes in conventional and super-resolution microscopy. More specifically, we discovered the physico-chemical properties of photoconvertible fluorescent probes, which I used to reconstruct the plasma membrane in STORM imaging on living cells. In the future, this will make it possible to follow the dynamics of spines during synaptic plasticity in STORM imaging. My results suggest the existence of an uncharacterized VAMP7-positive dendritic compartments, whose function would be to act as a storage station for synaptic proteins and receptors. It would be interesting to investigate whether the activity and trafficking of synaptic receptors would then be under the control of VAMP7 which could also be dependent on the level of synaptic activity. In this way, we could study VAMP7 exocytosis and how its activity is modulated during synaptic plasticity (LTP - LTD)
Chassefeyre, Romain. "Rôle de CHMP2B et du complexe ESCRT-III dans le remodelage dans membranes cellulaires : cas des épines dendritiques." Thesis, Grenoble, 2013. http://www.theses.fr/2013GRENV049/document.
CHMP2B is a subunit of ESCRT-III, a highly conserved cytosolic protein machinery, responsible for membrane remodeling in diverse cellular mechanisms. Mutations in CHMP2B are responsible for a familial form of frontotemporal dementia. A previous study highlighted that FTD-related mutants of CHMP2B impair the morphological maturation of dendritic spines, a process that may underlie neurodegeneration in this disease. The goal of this research work id directed towards understanding the role of CHMP2B and ESCRT-III in dendritic spines structure and function. In cell lines, we demonstrated that CHMP2B associates preferentially with the plasma membrane, polymerizes in helical filaments and forms long and thin membrane protrusions. This result indicates that CHMP2B is directly involved in plasma membrane remodeling. In neurons, CHMP2B concentrates in specific sub-membrane microdomains close to the PSD. Biochemical analysis revealed that CHMP2B and CHMP4B associate with other subunits to form a remarkably stable postsynaptic ESCRT-III complex. Mass-spectrometry indicated that this complex also interacts with postsynaptic scaffolds and proteins involved in actin cytoskeleton remodelling. RNAi depletion of CHMP2B, in cultured neurons, alters stability of dendrite branching and morphology of dendritic spines, and impairs spine head growth, normally associated with LTP. Rescue experiments, with point mutants, indicated that CHMP2B activity in dendrite branching is dependent on its capacity to both bind phospholipids and oligomerization with ESCRT-III. We propose a novel functionality for an ESCRT-III complex containing CHMP2B, in maturation-dependent and plasticity-dependent processes of dendritic spine morphogenesis
Belly, Agnès. "Régulation de la traduction des ARNm dendritiques par des ribonucléoprotéines et Rôle de CHMP2B dans la morphogenèse des épines dendritiques." Phd thesis, Grenoble 1, 2009. http://www.theses.fr/2009GRE10157.
Dendritic spines are highly dynamic small protusions of dendrites corresponding to the post-synaptic parts of excitatory synapses. Ln response to activity, spine shape and biochemical properties change, underling synaptic strength. These changes can be allowed by de novo synthesis from local RNAs and differential traffic of endocytosed synaptic receptors. We found that, in the brain, the ribonucleoprotein SaI regulate the translation of elongation factor eEF1A mRNA; and both in culture and in situ TLS can be relocalized from the nucleus to synapses. Using cultured hippocampal neurons, we found that CHMP2B mutants (member of endosomial complex ESCRT III and mutated in a neurodegenerative disease) affect dendritic spine morphology in that the proportion of large spines was reduced and reduce the amount of le: amplitude synaptic currents
Belly, Agnès. "Régulation de la traduction des ARNm dendritiques par des ribonucléoprotéines et rôle de CHMP2B dans la morphogenèse des épines dendritiques." Phd thesis, Université Joseph Fourier (Grenoble), 2009. http://tel.archives-ouvertes.fr/tel-00482920.
Chevy, Quentin. "Rôle du transporteur neuronal Potassium/Chlore KCC2 dans la plasticité des synapses glutamatergiques." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066041/document.
The polarity and efficacy of GABAergic synaptic transmission are both influenced by the intra-neuronal chloride concentration. In mature neurons, chloride extrusion through the neuronal K/Cl cotransporter KCC2 allows an inhibitory influx of chloride upon activation of GABAA receptors. Nevertheless, KCC2 is enriched in the vicinity of excitatory synapses within the dendritic spines that are actin-rich protrusions emerging from dendritic shafts. While it has become clear that KCC2 suppression alters chloride homeostasis and GABA signaling, little is known on its impact on glutamatergic transmission. In the laboratory, we have previously demonstrated that KCC2 suppression in mature neurons leads to decreased glutamatergic transmission efficacy through an ion-transport independent function of KCC2. During my PhD, I have explored how KCC2 may also impact LTP of glutamatergic synapses. My work reveals that KCC2 suppression compromises both functional and structural LTP at these synapses. This effect is associated with inhibition of the actin-severing protein cofilin and enhanced mobilization of F-actin in dendritic spines. Since LTP can be rescued by preventing cofilin inhibition upon KCC2 suppression, I suggest KCC2 might influence LTP through altered actin cytoskeleton dynamics. My results demonstrate that KCC2 function extends beyond the mere control of neuronal chloride homoeostasis and suggest regulation of KCC2 membrane stability may act as a metaplastic switch to gate long term plasticity at excitatory synapses in cortical neurons
Denizet, Marie. "Rôle de la microglie dans la neurogenèse adulte, dans le bulbe olfactif de la souris." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066391/document.
Microglia are resident immune cells in the central nervous system. They participate in the pruning of developing neurons. Complement factors are key markers of the dendritic spines to eliminate
Dollmeyer, Marc. "Etude des atteintes morphofonctionnelles des synapses excitatrices dans la maladie d'Alzheimer : implication de la voie Cofiline-dépendante." Thesis, Université Grenoble Alpes (ComUE), 2015. http://www.theses.fr/2015GREAV022/document.
Alzheimer's disease (AD) is a neurodegenerative pathology associated with progressive cerebral atrophy linked to neuronal death. It has been recently suggested that loss of cognitive functions occurring during the disease was a consequence of synapse dysfunction and prior to neuronal death. Thus, it has been observed that Amyloïd-β peptide (Aβ), the main component of senile plaques, one histological marker of the disease, also exists as soluble/oligomeric Aβ (Aβo). This Aβ conformation is known to be synaptotoxic. Aβo acts preferentially on the post-synaptic compartment of excitatory synapses, also named dendritic spines, sub-cellular micro-domains containing dynamic and filamentous actin as their main cytoskeleton component. Among numerous theories explaining Aβo synaptotoxicity, it has been suggested that spine collapsing was due to an abnormal actin depolymerisation through Cofilin enzyme. Yet, recent evidences inversely showed Cofilin phosphorylation/inactivation in frontal cortex of AD patients and in the APP/PS-1 transgenic mice brain, an AD animal model. Moreover, synapse morphological analysis in the CA1 region of APP/PS-1 mice showed a reduction in spine density and an increase in spine head volume of remaining ones. Spine head volume variations are commonly occurring during induction of Long Term Potentiation, the electrophysiological correlate of memory.During my thesis, we firstly characterized APP/PS-1 mice dendritic spine morphological alterations using electron microscopy. We confirmed that even at 3 month-old, excitatory synapses are fewer, but also that remaining ones display larger surfaces. In addition, PSD thickness is not proportional to spine surface anymore, which suggests an uncoupling between functional and morphological modifications. We also demonstrated the presence of abnormal shaped spinules onto spines.Using primary cortical neuron cultures, we demonstrated that acute Aβo treatment induces the formation of filamentous actin enriched protrusions, resembling spinules observed in transgenic mice. By purifying post-synaptic protein fraction, we showed that protrusions formation is correlated to an abnormal Cofilin phosphorylation/inactivation by Aβo. Thus, resulting Cofilin inactivation could trigger actin filament stabilization, leading to protrusion formation. We also found Cofilin phosphorylation in APP/PS-1 mice and in AD brains. Taken together, these results show that Aβo triggers dendritic spine abnormal alterations, characterized by the formation of membrane protrusions ressembling spinules. These protrusions are not activity-dependant, but may instead originate from a disregulation of Cofilin enzymatic activity by Aβo
Fol, Romain. "Conséquences de la surexpression des formes solubles de l’APP dans les mécanismes de mémoire : application à la maladie d'Alzheimer." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB047/document.
One of the main characteristic of Alzheimer’s Disease (AD) is the intracerebral accumulation of the neurotoxic Amyloid β peptide (Aβ) either as oligomeric or aggregated forms known as the amyloid plaques. This peptide is produced via the Amyloid Precursor Protein (APP) processing following the amyloidogenic pathway, pathological pathway overactivated in AD. Most of the research performed during the last 25 years focused on pathogenic consequences of this dysregulation, deprioritizing the understanding of the APP physiological functions. Nonetheless, numerous studies show that these physiological functions might be mediated via APP soluble forms (APPs). In the physiological APP processing pathway, the non-amyloidogenic pathway, APP is cleaved by the α secretase, releasing the APPsα which display neuroprotective and synaptotrophic properties, essential for brain normal functions. In the context of AD, the amyloidogenic pathway overactivation leads to APPsβ overproduction at the expense of APPsα. Therefore, AD harmful consequences could be due to the decrease of APPsα concentration associated with an increase of APPsβ. My thesis project aimed to characterize mnemonic and functional properties following the overexpression of these two soluble forms of APP and their therapeutic potential in AD. We firstly overexpressed APPsα in hippocampal neurons of APP/PS1ΔE9 mice, animal model of AD, which display cognitive and synaptic deficits. The continual expression of APPsα, mediated via AAV viruses, enabled restoration of spatial memory, long-term potentiation and dendritic spines density in the hippocampus. This phenotypic rescue was accompanied with the decrease of both Aβ levels and amyloid plaques. This might be due to the activation of microglia, cell type able to internalize and degrade Aβ. In a second hand, I studied the involvement of APPsβ in AD, which remains poorly known. Its overexpression in APP/PS1ΔE9 did not induce neither LTP nor spatial memory restoration. However, APPsβ injection lead to the decrease of Aβ levels without reducing amyloid plaques. This default might be due to the lack of microglial activation. In conclusion, my thesis work show that, unlike APPsβ, APPsα overexpression might overcome the AD inevitable evolution by reducing synaptic and memory alterations, typical of AD. These results reinforce a new way of treatment to cope with AD progression. The use of APPsα as therapeutic agent might be an important tool for future AD therapies