Littérature scientifique sur le sujet « GABA, glutamate,synapses »
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Articles de revues sur le sujet "GABA, glutamate,synapses"
Khatri, Shailesh N., Wan-Chen Wu, Ying Yang et Jason R. Pugh. « Direction of action of presynaptic GABAA receptors is highly dependent on the level of receptor activation ». Journal of Neurophysiology 121, no 5 (1 mai 2019) : 1896–905. http://dx.doi.org/10.1152/jn.00779.2018.
Texte intégralGundersen, Vidar, Frode Fonnum, Ole Petter Ottersen et Jon Storm-Mathisen. « Redistribution of Neuroactive Amino Acids in Hippocampus and Striatum during Hypoglycemia : A Quantitative Immunogold Study ». Journal of Cerebral Blood Flow & ; Metabolism 21, no 1 (janvier 2001) : 41–51. http://dx.doi.org/10.1097/00004647-200101000-00006.
Texte intégralKaneda, Katsuyuki, et Hitoshi Kita. « Synaptically Released GABA Activates Both Pre- and Postsynaptic GABAB Receptors in the Rat Globus Pallidus ». Journal of Neurophysiology 94, no 2 (août 2005) : 1104–14. http://dx.doi.org/10.1152/jn.00255.2005.
Texte intégralDeFazio, R. Anthony, Ami P. Raval, Hung W. Lin, Kunjan R. Dave, David Della-Morte et Miguel A. Perez-Pinzon. « GABA Synapses Mediate Neuroprotection after Ischemic and εPKC Preconditioning in Rat Hippocampal Slice Cultures ». Journal of Cerebral Blood Flow & ; Metabolism 29, no 2 (29 octobre 2008) : 375–84. http://dx.doi.org/10.1038/jcbfm.2008.126.
Texte intégralWalls, Anne B., Elvar M. Eyjolfsson, Olav B. Smeland, Linn Hege Nilsen, Inger Schousboe, Arne Schousboe, Ursula Sonnewald et Helle S. Waagepetersen. « Knockout of GAD65 has Major Impact on Synaptic GABA Synthesized from Astrocyte-Derived Glutamine ». Journal of Cerebral Blood Flow & ; Metabolism 31, no 2 (28 juillet 2010) : 494–503. http://dx.doi.org/10.1038/jcbfm.2010.115.
Texte intégralLiao, Fei, Haitao Liu, Santiago Milla-Navarro, Pedro de la Villa et Francisco Germain. « Origin of Retinal Oscillatory Potentials in the Mouse, a Tool to Specifically Locate Retinal Damage ». International Journal of Molecular Sciences 24, no 4 (4 février 2023) : 3126. http://dx.doi.org/10.3390/ijms24043126.
Texte intégralYamamoto, Ryo, Takafumi Furuyama, Tokio Sugai, Munenori Ono, Denis Pare et Nobuo Kato. « Serotonergic control of GABAergic inhibition in the lateral amygdala ». Journal of Neurophysiology 123, no 2 (1 février 2020) : 670–81. http://dx.doi.org/10.1152/jn.00500.2019.
Texte intégralSethuramanujam, Santhosh, et Malcolm M. Slaughter. « Disinhibitory recruitment of NMDA receptor pathways in retina ». Journal of Neurophysiology 112, no 1 (1 juillet 2014) : 193–203. http://dx.doi.org/10.1152/jn.00817.2013.
Texte intégralChéry, Nadège, et Yves De Koninck. « GABAB Receptors Are the First Target of Released GABA at Lamina I Inhibitory Synapses in the Adult Rat Spinal Cord ». Journal of Neurophysiology 84, no 2 (1 août 2000) : 1006–11. http://dx.doi.org/10.1152/jn.2000.84.2.1006.
Texte intégralAroniadou-Anderjaska, Vassiliki, Fu-Ming Zhou, Catherine A. Priest, Matthew Ennis et Michael T. Shipley. « Tonic and Synaptically Evoked Presynaptic Inhibition of Sensory Input to the Rat Olfactory Bulb Via GABABHeteroreceptors ». Journal of Neurophysiology 84, no 3 (1 septembre 2000) : 1194–203. http://dx.doi.org/10.1152/jn.2000.84.3.1194.
Texte intégralThèses sur le sujet "GABA, glutamate,synapses"
Monassier, Laurent. « Approche pharmacologique de la modulation des synapses glutamatergiques du systeme nerveux sympathique : une cible pour des drogues cardioprotectrices ? » Strasbourg 1, 1997. http://www.theses.fr/1997STR15026.
Texte intégralPin, Jean-Philippe. « Interaction glutamate/GABA : mécanismes et pharmacologie de la libération de GABA des neurones de striatum en culture primaire : effets des acides aminés excitateurs ». Montpellier 2, 1987. http://www.theses.fr/1987MON20211.
Texte intégralBoulland, Jean-Luc. « Recycling the amino acid neurotransmitter glutamate in the CNS : l'alchimie du glutamate et de la glutamine ». Paris 6, 2004. http://www.theses.fr/2004PA066017.
Texte intégralEl, Khoury Rita. « Deux syndromes, un même gène : conséquences d'un mauvais dosage de MeCP2 sur la transmission synaptique et le comportement chez la souris ». Thesis, Aix-Marseille, 2013. http://www.theses.fr/2013AIXM5075.
Texte intégralMeCP2 is a multifunctional protein acting on many levels of control of genetic programs. Thus, an abnormal dosage of MeCP2 protein causes a group of neurological disorders with a common feature of severe intellectual disability. Mutations or deletions in MECP2 gene cause Rett Syndrome in females, whereas in boys its overexpression causes the MECP2-duplication Syndrome. Several mouse models of MECP2-pathologies were generated. The use of these models is crucial for understanding the mechanisms underlying the onset of symptoms related to the pathology. In our laboratory, two mouse models are under study: The Mecp2tm1Bird model with an Mecp2 deficiency and the transgenic Mecp2Tg1 model with a double expression of Mecp2. My thesis work enabled the characterization of the postnatal physiological and motor deficits affecting Mecp2Tg1 mice. My work led to a better understanding of the gene dosage effect. Our results showed that overexpression of Mecp2 in mice, led to the occurrence of motor problems, and seizures. In parallel, we studied the neural deficits affecting the GABA and the glutamate pathway in several structures of the Mecp2 deficient brain (Mecp2tm1bird). We showed that Mecp2-deficiency causes deregulation of the synaptic transmission, which is dependent on the area, and the age of the study. These deregulations underlie significant neurophysiological differences between the different regions of the brain that we still have to uncover. Furthermore, we found that pharmacological stimulation of the GABA system with Tiagabine, a molecule capable of acting on GABA transporters to prevent its uptake, increases the survival of Mecp2-deficients animals
Malinina, Evgenya. « Neurotransmission and functional synaptic plasticity in the rat medial preoptic nucleus ». Doctoral thesis, Umeå : Umeå university, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-25874.
Texte intégralPiot, Laura. « Nouveaux éléments sur la structure, fonction et pharmacologie des récepteurs delta (GluD) ». Thesis, Sorbonne université, 2021. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2021SORUS522.pdf.
Texte intégralIonotropic glutamate receptors (iGluRs) are the main mediators of excitatory transmission in the vertebrate central nervous system (CNS). It has long been considered that the biological responses elicited by iGluRs were necessarily related to the flow of ions through their channel, hence the name "ionotropic". However, many data indicate that several members of this class of receptors can induce intracellular signaling without opening their channel. This is the case of delta receptors, a class comprising two members (GluD1 and GluD2) which plays key roles in synapse formation and the regulation of synaptic transmission through non-ionotropic signaling. However, the molecular mechanisms of GluD receptor function and signaling, as well as their pharmacology, still remain poorly understood, due to a lack of appropriate tools for their study. During my thesis, I developed two methods to study GluD1 receptors: (i) a constitutively open mutant allowing the study of GluD1 by classical cell electrophysiology, and (ii) a fluorescence technique called 'voltage-clamp fluorometry' or VCF to detect in real time local conformational changes within GluD1. These tools offer an unprecedented means to study the pharmacology and molecular mechanisms of signal transduction in this class of receptors. I was thus able to characterize and quantify the sensitivity of GluD1 receptors to a series of synthetic and natural ligands
Tora, Amélie. « Modulation endogène des récepteurs métabotropiques du glutamate : bases moléculaires et implications fonctionnelles de la sensibilité au chlore extracellulaire ». Thesis, Montpellier, 2015. http://www.theses.fr/2015MONTT032.
Texte intégralMetabotropic glutamate receptors (mGluRs) are G coupled-protein receptors (GPCRs) playing key roles in synaptic transmission in the central nervous system. They display a large extracellular domain, the Venus Flytrap (VFT) where the endogenous ligand, glutamate, binds. Their 7 transmembrane helices spanning domain, common to all GPCRs, is known to be the target of new therapeutic compounds, called allosteric modulators. In contrast, VFT domain is used to develop glutamate competitive ligands and there are only few data about allosteric modulators targeting the VFT. Recent studies have shown mGluRs are sensitive to extracellular ions, particularly to chloride (Cl-), although its binding site has not been elucidated. This thesis work explores the possibility of an endogenous allosteric modulation of mGluRs by Cl-, aiming to delineate its binding site(s) and its effect on receptor conformational dynamics and function. Using pharmacological, FRET based biophysical approaches and modelling, we have first confirmed that Cl- potentiates glutamate action in all mGluRs and that this ion favors agonist induced active conformation by binding to the VFT. mGluRs are also differently sensitive to Cl-, mGlu4 being the most and mGlu2 the least. This difference is notably explained by the number of Cl- functional sites within the VFT, all mGluRs including mGlu4 displaying 2 sites per monomer whereas mGlu2 has only 1 site due to a serine-aspartate “key” mutation in VFT lobe 1. Besides, mGlu3 receptor appears to be a “special case”, as this receptor is highly sensitive to Cl- because its VFT domain is carrying amino acids creating a “Cl- lock”, which dramatically favors active conformation and a high level of basal activity. Finally, modelling of extracellular Cl- concentration variations in a GABAergic synapse is compatible with a modulation of the most sensitive mGluRs. In conclusion, Cl- is an endogenous allosteric modulator of mGluRs and exploiting its binding sites may yield to the development of innovative therapeutic tools
Majdoubi, Mohammed el. « Etude neuroanatomique des innervations des neurones magnocellulaires à ocytocine et à vasopressine et de leur contribution à la plasticité synaptique induite par l'allaitement ». Bordeaux 2, 1996. http://www.theses.fr/1996BOR28435.
Texte intégralChapitres de livres sur le sujet "GABA, glutamate,synapses"
Gillespie, Deda C., et Karl Kandler. « GABA, Glycine, and Glutamate Co-Release at Developing Inhibitory Synapses ». Dans Co-Existence and Co-Release of Classical Neurotransmitters, 1–26. Boston, MA : Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-09622-3_5.
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