Littérature scientifique sur le sujet « GABAergic/glycinergic synaptic transmission »
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Articles de revues sur le sujet "GABAergic/glycinergic synaptic transmission"
Donato, Roberta, et Andrea Nistri. « Relative Contribution by GABA or Glycine to Cl−-Mediated Synaptic Transmission on Rat Hypoglossal Motoneurons In Vitro ». Journal of Neurophysiology 84, no 6 (1 décembre 2000) : 2715–24. http://dx.doi.org/10.1152/jn.2000.84.6.2715.
Texte intégralDonato, Roberta, et Andrea Nistri. « Differential Short-Term Changes in GABAergic or Glycinergic Synaptic Efficacy on Rat Hypoglossal Motoneurons ». Journal of Neurophysiology 86, no 2 (1 août 2001) : 565–74. http://dx.doi.org/10.1152/jn.2001.86.2.565.
Texte intégralAwatramani, Gautam B., Rostislav Turecek et Laurence O. Trussell. « Staggered Development of GABAergic and Glycinergic Transmission in the MNTB ». Journal of Neurophysiology 93, no 2 (février 2005) : 819–28. http://dx.doi.org/10.1152/jn.00798.2004.
Texte intégralSebe, Joy Y., Erika D. Eggers et Albert J. Berger. « Differential Effects of Ethanol on GABAA and Glycine Receptor-Mediated Synaptic Currents in Brain Stem Motoneurons ». Journal of Neurophysiology 90, no 2 (août 2003) : 870–75. http://dx.doi.org/10.1152/jn.00119.2003.
Texte intégralLiu, Tao, Tsugumi Fujita et Eiichi Kumamoto. « Acetylcholine and norepinephrine mediate GABAergic but not glycinergic transmission enhancement by melittin in adult rat substantia gelatinosa neurons ». Journal of Neurophysiology 106, no 1 (juillet 2011) : 233–46. http://dx.doi.org/10.1152/jn.00838.2010.
Texte intégralSchubert, Timm, Daniel Kerschensteiner, Erika D. Eggers, Thomas Misgeld, Martin Kerschensteiner, Jeff W. Lichtman, Peter D. Lukasiewicz et Rachel O. L. Wong. « Development of Presynaptic Inhibition Onto Retinal Bipolar Cell Axon Terminals Is Subclass-Specific ». Journal of Neurophysiology 100, no 1 (juillet 2008) : 304–16. http://dx.doi.org/10.1152/jn.90202.2008.
Texte intégralLiu, Tao, Tsugumi Fujita, Terumasa Nakatsuka et Eiichi Kumamoto. « Phospholipase A2 Activation Enhances Inhibitory Synaptic Transmission in Rat Substantia Gelatinosa Neurons ». Journal of Neurophysiology 99, no 3 (mars 2008) : 1274–84. http://dx.doi.org/10.1152/jn.01292.2007.
Texte intégralGao, Bao-Xi, Christian Stricker et Lea Ziskind-Conhaim. « Transition From GABAergic to Glycinergic Synaptic Transmission in Newly Formed Spinal Networks ». Journal of Neurophysiology 86, no 1 (1 juillet 2001) : 492–502. http://dx.doi.org/10.1152/jn.2001.86.1.492.
Texte intégralMcMenamin, Caitlin A., Laura Anselmi, R. Alberto Travagli et Kirsteen N. Browning. « Developmental regulation of inhibitory synaptic currents in the dorsal motor nucleus of the vagus in the rat ». Journal of Neurophysiology 116, no 4 (1 octobre 2016) : 1705–14. http://dx.doi.org/10.1152/jn.00249.2016.
Texte intégralShao, Mei, June C. Hirsch et Kenna D. Peusner. « Emergence of Action Potential Generation and Synaptic Transmission in Vestibular Nucleus Neurons ». Journal of Neurophysiology 96, no 3 (septembre 2006) : 1215–26. http://dx.doi.org/10.1152/jn.00180.2006.
Texte intégralThèses sur le sujet "GABAergic/glycinergic synaptic transmission"
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.
Texte intégralAmyotrophic 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
Mellor, Jack Robert. « Electrophysiological investigation of the mechanisms underlying GABAergic synaptic transmission ». Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624122.
Texte intégralSinger, Joshua H. « Postnatal development of glycinergic synaptic transmission and biophysical properties of glycine receptor-channels / ». Thesis, Connect to this title online ; UW restricted, 1998. http://hdl.handle.net/1773/10535.
Texte intégralFan, Kai Yoon. « GABAergic synaptic transmission, plasticity and integration in the subthalamic nucleus ». Thesis, University of Sheffield, 2012. http://etheses.whiterose.ac.uk/3167/.
Texte intégralAntonelli, Roberta. « The role of prolyl-isomerase PIN1 in GABAergic and glutamatergic synaptic transmission ». Doctoral thesis, SISSA, 2015. http://hdl.handle.net/20.500.11767/4893.
Texte intégralYuan, Ning. « DISTINCT MODULATORY EFFECTS OF DOPAMINE ON EXCITATORY CHOLINERGIC AND INHIBITORY GABAERGIC SYNAPTIC TRANSMISSION IN DROSOPHILA ». Ohio University / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1149001533.
Texte intégralAyling, Martin D. T. « A computational analysis of the functional role of GABAergic synaptic transmission in striatal medium spiny neurons ». Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.491856.
Texte intégralDiana, Marco Alberto. « Charakterisierung von einer retrograden Modulation inhibitorischer synaptischer Transmission im Kleinhirn der Ratte ». Doctoral thesis, [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=971021988.
Texte intégralWerner, Christian [Verfasser], Claudia [Gutachter] Sommer, Marie-Christine [Gutachter] Dabauvalle et Erhard [Gutachter] Wischmeyer. « Effect of autoantibodies targeting amphiphysin or glutamate decarboxylase 65 on synaptic transmission of GABAergic neurons / Christian Werner. Gutachter : Claudia Sommer ; Marie-Christine Dabauvalle ; Erhard Wischmeyer ». Würzburg : Universität Würzburg, 2014. http://d-nb.info/1108780873/34.
Texte intégralDonato, 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.
Texte intégralNeocortical 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
Livres sur le sujet "GABAergic/glycinergic synaptic transmission"
Giovanni, Biggio, Concas Alessandra et Costa Erminio, dir. GABAergic synaptic transmission : Molecular, pharmacological, and clinical aspects. New York : Raven Press, 1992.
Trouver le texte intégralL, Alkon Daniel, et National Institute of Neurological and Communicative Disorders and Stroke, dir. Long-term transformation of an inhibitory into an excitatory GABAergic synaptic response. [Bethesda, Md. ? : National Institute of Neurological and Communicative Disorders and Stroke, 1993.
Trouver le texte intégralBiggio, Giovanni, et Alessandra Concas. Gabaergic Synaptic Transmission : Molecular, Pharmacological, and Clinical Aspects (Advances in Biochemical Psychopharmacology). Raven Pr, 1992.
Trouver le texte intégralGiovanni, Giuseppe Di, Adam C. Errington et Vincenzo Crunelli. Extrasynaptic GABAA Receptors. Springer, 2014.
Trouver le texte intégralGiovanni, Giuseppe Di, Adam C. Errington et Vincenzo Crunelli. Extrasynaptic GABAA Receptors. Springer, 2016.
Trouver le texte intégralGiovanni, Giuseppe Di, Adam C. Errington et Vincenzo Crunelli. Extrasynaptic GABAA Receptors. Springer, 2014.
Trouver le texte intégralChapitres de livres sur le sujet "GABAergic/glycinergic synaptic transmission"
Dieudonné, Stéphane, et Marco Alberto Diana. « Postsynaptic Determinants of Inhibitory Transmission at Mixed GABAergic/Glycinergic Synapses ». Dans Co-Existence and Co-Release of Classical Neurotransmitters, 1–27. Boston, MA : Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-09622-3_7.
Texte intégralGaiarsa, Jean-Luc, et Yezekiel Ben-Ari. « Ontogenesis of Gabaergic and Glutamatergic Synaptic Transmission ». Dans Advances in Behavioral Biology, 45–54. Boston, MA : Springer US, 2001. http://dx.doi.org/10.1007/0-306-47612-6_5.
Texte intégralWoodin, Melanie A., et Mu-ming Poo. « Activity-Dependent Modification of Cation-Chloride Cotransporters Underlying Plasticity of Gabaergic Synaptic Transmission ». Dans Excitatory-Inhibitory Balance, 89–97. Boston, MA : Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0039-1_6.
Texte intégralYazawa, Tohru, et Kiyoaki Kuwasawa. « Cholinergic, Catecholaminergic and Gabaergic Mechanisms of Synaptic Transmission in the Heart of the Hermit Crab ». Dans Frontiers in Crustacean Neurobiology, 401–6. Basel : Birkhäuser Basel, 1990. http://dx.doi.org/10.1007/978-3-0348-5689-8_49.
Texte intégralMori, Akihisa, Tomomi Shindou, Michio Ichimura, Hiromi Nonaka et Hiroshi Kase. « The Role of Adenosine A2a Receptors in Regulating Gabaergic Synaptic Transmission in Striatal Medium Spiny Neurons ». Dans Advances in Behavioral Biology, 119–22. Boston, MA : Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-0194-1_13.
Texte intégralDraguhn, Andreas, et Kristin Hartmann. « GABAergic Synaptic Transmission ». Dans Advances in Molecular and Cell Biology, 215–40. Elsevier, 2006. http://dx.doi.org/10.1016/s1569-2558(06)38009-5.
Texte intégralFeltz, Anne. « Fast Synaptic Transmission : Nicotinic and GABAergic Transmissions ». Dans Physiology of Neurons, 133–68. Garland Science, 2020. http://dx.doi.org/10.1201/9780429292972-6.
Texte intégralBenarroch, Eduardo E. « Inhibitory Amino Acid Neurotransmission and Synaptopathies ». Dans Neuroscience for Clinicians, sous la direction de Eduardo E. Benarroch, 317–36. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.003.0018.
Texte intégralKano, Masanobu. « Long-lasting potentiation of GABAergic inhibitory synaptic transmission in cerebellar Purkinje cells : Its properties and possible mechanisms ». Dans Motor Learning and Synaptic Plasticity in the Cerebellum, 16–23. Cambridge University Press, 1997. http://dx.doi.org/10.1017/cbo9780511666896.004.
Texte intégralPavel, Osten, Wisden William et Sprengel Rolf. « Molecular Mechanisms of Synaptic Function in the Hippocampus : Neurotransmitter Exocytosis and Glutamatergic, GABAergic, and Cholinergic Transmission ». Dans The Hippocampus Book, 243–96. Oxford University Press, 2006. http://dx.doi.org/10.1093/acprof:oso/9780195100273.003.0007.
Texte intégralActes de conférences sur le sujet "GABAergic/glycinergic synaptic transmission"
Li, Guoshi, Stacy Cheng, Frank Ko, Scott L. Raunch, Gregory Quirk et Satish S. Nair. « Computational Modeling of Lateral Amygdala Neurons During Acquisition and Extinction of Conditioned Fear, Using Hebbian Learning ». Dans ASME 2006 International Mechanical Engineering Congress and Exposition. ASMEDC, 2006. http://dx.doi.org/10.1115/imece2006-15078.
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