Добірка наукової літератури з теми "Transmission synaptique GABAergic/glycinergique"
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Дисертації з теми "Transmission synaptique GABAergic/glycinergique"
Zhu, Hongmei. "Prenatal dysfunctions of chloride-related inhibition in lumbar motoneurons of the SOD1G93A ALS." Electronic Thesis or Diss., Bordeaux, 2023. http://www.theses.fr/2023BORD0026.
Повний текст джерелаAmyotrophic lateral sclerosis (ALS) is a fatal and adult-onset neurodegenerative disease characterized by a progressive degeneration of motoneurons (MNs) with complex multifactorial aetiology. Most ALS studies have focused on symptomatic stages based on the hypothesis that ALS pathogenesis occurs when the disease becomes symptomatic. However, growing evidence indicates that ALS pathogenesis might start long before symptom onset. My PhD thesis work was based on the hypothesis that ALS - familial and sporadic - stems from deficits taking place during early development. With the aim of identifying early changes underpinning ALS neurodegeneration, the first part of my thesis analysed the GABAergic/glycinergic inhibitory postsynaptic currents (IPSCs) to embryonic (E) E17.5 MNs located in the ventro-lateral motor column from SOD1G93A (SOD) mice, in parallel with the analyse of chloride homeostasis. Our results showed that IPSCs are less frequent in SOD animals in accordance with a reduction of synaptic VIAAT-positive terminals in the close proximity of MN somata. SOD MNs exhibited an ECI 10 mV more depolarized than wild type (WT) MNs. This deficit in GABA/glycine inhibition was due to a reduction of the neuronal chloride transporter KCC2. SOD spontaneous IPSCs and evoked GABAAR-currents exhibited a slower decay correlated to elevated [Cl-]i. Using computer modelling approach, we revealed that the slower relaxation of synaptic inhibitory events acts as a compensatory mechanism to strengthen or increase the efficacy of GABA/glycine inhibition when ECI is more depolarized. Interestingly, simulations revealed an excitatory effect of low frequency (<50Hz) depolarizing GABA/glycine post-synaptic potentials (dGPSPs) in SOD-like MNs but not in WT-like littermates. At high frequency, dGPSPs switched to inhibitory effect resulting from the summation of the shunting components. The second part of my PhD thesis focussed on the effect of electrically evoked-dGPSPs, at different frequencies (7.5 to 100 Hz), on real lumbar E17.5 MNs in which a depolarized ECI (below spike threshold) was imposed. The aim was to examine whether the excitatory effect could be linked to morphological changes previously described in E17.5 SOD MNs. Results showed that some MNs were excited by low frequency dGPSPs and inhibited by high frequency dGPSPs (Dual MNs) and others were inhibited at all frequencies (Inhibited MNs). Dual effect was more often detected in SOD MNs. WT MNs were classified into two clusters according to their input resistance (Rin), Dual MNs being specific to high Rin and Inhibited MNs to low Rin. Morphometric data pointed out a reduced dendritic tree in high Rin WT Dual MNs and a large dendritic tree in low Rin Inhibited MNs. This was not the case in SOD MNs that were excited or inhibited whatever their morphology and Rin. In agreement with simulation showing that a less density of inhibitory current on MNs soma favours excitatory dGPSPs, we found less synaptic VIAAT terminals on the soma and proximal dendrites of SOD MNs, compared to littermate WT MNs, as well as a lower frequency of spontaneous dGPSPs. Altogether, my thesis data emphasize a prenatal defect in the CI- homeostasis and GABA/glycine innervation in the SOD1G93A ALS MNs. Before birth, a dominant population of MNs with low Rin emerges in WT animals. These MNs that are inhibited by dGPSPs could represent future ALS vulnerable fast MNs (putative FF). Interestingly, those MNs are not inhibited in SOD animals. The inhibitory dysfunction could be attributed to two distinct factors: morphology and perisomatic inhibitory synapse density. Of these two factors, the latter plays a major role by controlling capability of GABAergic/glycinergic neurons for shaping spinal motor output
Zell, Vivien. "Impact des glucocorticoïdes circulants sur la maturation et le fonctionnement de l'inhibition spinale GABAergique." Thesis, Strasbourg, 2013. http://www.theses.fr/2013STRAJ097/document.
Повний текст джерелаGlucocorticoids (GC) are steroid hormones synthesized in adrenals following HPA axis activation. GC production is a response of the organism to alleviate homeostasis perturbations through different actions. One of them involves central neuronal modulation of behavior and pain perception.Primary afferents convey peripheral sensory information in the dorsal horns of the spinal cord. This information can be nociceptive and are modulated by a spinal neuronal network before being transmitted and integrated. We showed that GC are implied in the maturation and functioning of the inhibitory transmission involving GABA neurotransmitter. In the dorsal horns this inhibitory transmission is of major importance, limiting the processing of nociceptive information
Donato, Cristina. "Synaptic identity of neocortical circuits involving Martinotti cells in healthy conditions and in Down syndrome." Thesis, Sorbonne université, 2019. https://accesdistant.sorbonne-universite.fr/login?url=http://theses-intra.upmc.fr/modules/resources/download/theses/2019SORUS079.pdf.
Повний текст джерелаNeocortical GABAergic interneurons encompass a vast number of cell types: some innervate the perisomatic region of cortical pyramidal neurons (PNs), whereas others target PN dendrites. Here we studied the alpha5 subunit of the GABAAR, which is believed to contribute significantly to tonic inhibition. We found that, in L 2/3 PNs of mouse somatosensory cortex, alpha5 provides a negligible contribution to tonic inhibition. Conversely, we found that alpha5 is specifically expressed at synapses between the dendrite-targeting interneurons Martinotti cells (MCs) thus indicating that GABAergic transmission through 5-GABAAR subtypes is important for synaptic dendritic inhibition. We also show that the expression of alpha5 is always present only at synapses made by MCs onto PNs. These results suggest alpha5-GABAARs as a molecular signature of specific inhibitory dendritic synapses involving MCs. Importantly, many brain diseases originate from dysfunctions of distinct inhibitory circuits and, in particular, alpha5-KO mice show improved learning: it was shown that the treatment with a highly specific alpha5 inverse agonist rescued learning and memory deficits in Ts65Dn mice, an animal model for Down syndrome (DS). Yet, the actual mechanisms underlying this cognitive rescue at the synaptic and circuit levels are unknown. Our preliminary results indicate that GABAergic synapses from dendrite-targeting MCs are specifically altered in DS. We are defining whether this alteration is circuit-specific. Our results will provide a better understanding of specific circuit alterations in DS, and will likely open new therapeutic avenues to alleviate cognitive impairment of this disease
Özcan, Orçun Orkan. "Characterization of the Purkinje cell to nuclear cell connections in mice cerebellum." Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAJ085/document.
Повний текст джерелаThe cerebellum integrates motor commands with somatosensory, vestibular, visual and auditory information for motor learning and coordination functions. The deep cerebellar nuclei (DCN) generates the final output by processing inputs from Purkinje cells (PC), mossy and climbing fibers. We investigated the properties of PC connections to DCN cells using optogenetic stimulation in L7-ChR2 mice with in vivo multi electrode extracellular recordings in lobule IV/V of the cerebellar cortex and in the medial nuclei. DCN cells discharged phase locked to local field potentials in the beta, gamma and high frequency bands. We identified two groups of DCN cells with significant differences in action potential waveforms and firing rates, matching previously discriminated in vitro properties of GABAergic and non-GABAergic cells. PCs inhibited the two group of cells gradually (rate coding), however spike times were controlled for only non-GABAergic cells. Our results suggest that PC inputs temporally control the output of cerebellum and the internal DCN circuitry supports this phenomenon since GABAergic cells do not induce a temporal effect through local inhibition
Xing, Paul. "Implication de Syngap1 dans la transmission GABAergique et la plasticité synaptique." Thèse, 2015. http://hdl.handle.net/1866/13793.
Повний текст джерелаIntellectual disability affects 1-3% of the world population, which make it the most common cognitive disorder of childhood. Our group discovered that mutation in the SYNGAP1 gene was a frequent cause of non-syndromic intellectual disability, accounting for 1-3% of the cases. For example, the fragile X syndrome, which is the most common monogenic cause of intellectual disability, accounts for 2% of all cases. Some patients affected by SYNGAP1 also showed autism spectrum disorder and epileptic seizures. Our group also showed that mutations in SYNGAP1 caused intellectual disability by an haploinsufficiency mechanism. SYNGAP1 codes for a protein expressed only in the brain which interacts with the GluN2B subunit of NMDA glutamatergic receptors (NMDAR). SYNGAP1 possesses a Ras-GAP activating activity which negatively regulates Ras at excitatory synapses. Heterozygote mice for Syngap1 (Syngap1+/- mice) show behaviour abnormalities and learning deficits, which makes them a good model of intellectual disability. Some studies showed that Syngap1 affects the brain development by perturbing the activity and plasticity of excitatory neurons. The excitatory/inhibitory imbalance is an emerging theory of the origin of intellectual disability and autism. However, some groups including ours, showed that Syngap1 is expressed in at least a subpopulation of GABAergic interneurons. Therefore, our hypothesis was that Syngap1 happloinsufficiency in interneurons contributes in part to the cognitive deficits and excitation/inhibition imbalance observed in Syngap1+/- mice. To test this hypothesis, we generated a transgenic mouse model where Syngap1 expression was decreased only in GABAergic interneurons derived from the medial ganglionic eminence, which expresses the transcription factor Nkx2.1 (Tg(Nkx2,1-Cre);Syngap1 mouse). We showed that miniature inhibitory postsynaptic currents (mIPSCs) were decreased in pyramidal cells in layers 2/3 in primary somatosensory cortex (S1) and in CA1 region of the hippocampus of Tg(Nkx2,1-Cre);Syngap1 mice. Those results suggest that Syngap1 haploinsufficiency in GABAergic interneurons contributes in part to the excitation/inhibition imbalance observed in Syngap1+/- mice. Interestingly, we also observed that miniature excitatory postsynaptic currents (mEPSCs) were increased in cortex S1 but decreased in CA1 region of the hippocampus. We further tested whether synaptic plasticity mechanisms that are thought to underlie learning and memory were affected by Syngap1 haploinsufficiency in GABAergic interneurons. We showed that NMDAR-dependent long-term potentiation (LTP) but not NMDAR-dependent long-term depression (LTD) was decreased in Tg(Nkx2,1-Cre);Syngap1 mice. We also showed that GABAA receptor blockade rescued in part the LTP deficit in Syngap1+/- mice, suggesting that a disinhibition deficit is present in these mice. Altogether, the results support a functional role of Syngap1 in GABAergic interneurons, which may in turn contributes to the deficit observed in Syngap1+/- mice.