Relevant bibliographies by topics / GABA, glutamate,synapses

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters

Academic literature on the topic 'GABA, glutamate,synapses'

Author: Grafiati
Published: 14 March 2023
Last updated: 31 July 2025

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Journal articles on the topic "GABA, glutamate,synapses"

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Khatri, Shailesh N., Wan-Chen Wu, Ying Yang, and 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 (2019): 1896–905. http://dx.doi.org/10.1152/jn.00779.2018.

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Many synapses, including parallel fiber synapses in the cerebellum, express presynaptic GABAA receptors. However, reports of the functional consequences of presynaptic GABAA receptor activation are variable across synapses, from inhibition to enhancement of transmitter release. We find that presynaptic GABAA receptor function is bidirectional at parallel fiber synapses depending on GABA concentration and modulation of GABAA receptors in mice. Activation of GABAA receptors by low GABA concentrations enhances glutamate release, whereas activation of receptors by higher GABA concentrations inhibi
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Gundersen, Vidar, Frode Fonnum, Ole Petter Ottersen, and 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 (2001): 41–51. http://dx.doi.org/10.1097/00004647-200101000-00006.

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Postembedding immunocytochemistry was used to localize aspartate, glutamate, gamma-aminobutyric acid (GABA), and glutamine in hippocampus and striatum during normo- and hypoglycemia in rat. In both brain regions, hypoglycemia caused aspartatelike immunoreactivity to increase. In hippocampus, this increase was evident particularly in the terminals of known excitatory afferents—in GABA-ergic neurons and myelinated axons. Aspartate was enriched along with glutamate in nerve terminals forming asymmetric synapses on spines and with GABA in terminals forming symmetric synapses on granule and pyramid
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Kaneda, Katsuyuki, and Hitoshi Kita. "Synaptically Released GABA Activates Both Pre- and Postsynaptic GABAB Receptors in the Rat Globus Pallidus." Journal of Neurophysiology 94, no. 2 (2005): 1104–14. http://dx.doi.org/10.1152/jn.00255.2005.

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The globus pallidus (GP) contains abundant GABAergic synapses and GABAB receptors. To investigate whether synaptically released GABA can activate pre- and postsynaptic GABAB receptors in the GP, physiological recordings were performed using rat brain slice preparations. Cell-attached recordings from GABAA antagonist-treated preparations revealed that repetitive local stimulation induced a GABAB antagonist-sensitive pause in spontaneous firings of GP neurons. Whole cell recordings revealed that the repetitive stimulation evoked fast excitatory postsynaptic potentials followed by a slow inhibito
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DeFazio, R. Anthony, Ami P. Raval, Hung W. Lin, Kunjan R. Dave, David Della-Morte та 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, № 2 (2008): 375–84. http://dx.doi.org/10.1038/jcbfm.2008.126.

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Delayed neuroprotection against ischemic challenges is conferred by both ischemic preconditioning (IPC) and preconditioning by activation of the ε-isoform of protein kinase C (εPKC-PC). In vivo, ischemic preconditioning enhances GABA release and ameliorates glutamate release during lethal cerebral ischemia. We tested the hypothesis that IPC and εPKC-PC confer neuroprotection by GABA synapses in rat organotypic hippocampal slices. Ischemic preconditioning or εPKC-PC was induced with 15 mins oxygen-glucose deprivation (OGD) or ψεRACK, a selective εPKC activator; and test ischemia consisted of 40
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Walls, Anne B., Elvar M. Eyjolfsson, Olav B. Smeland, et al. "Knockout of GAD65 has Major Impact on Synaptic GABA Synthesized from Astrocyte-Derived Glutamine." Journal of Cerebral Blood Flow & Metabolism 31, no. 2 (2010): 494–503. http://dx.doi.org/10.1038/jcbfm.2010.115.

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γ-Aminobutyric acid (GABA) synthesis from glutamate is catalyzed by glutamate decarboxylase (GAD) of which two isoforms, GAD65 and GAD67, have been identified. The GAD65 has repeatedly been shown to be important during intensified synaptic activity. To specifically elucidate the significance of GAD65 for maintenance of the highly compartmentalized intracellular and intercellular GABA homeostasis, GAD65 knockout and corresponding wild-type mice were injected with [1-13C]glucose and the astrocyte-specific substrate [1,2-13C]acetate. Synthesis of GABA from glutamine in the GABAergic synapses was
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Liao, Fei, Haitao Liu, Santiago Milla-Navarro, Pedro de la Villa, and 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 (2023): 3126. http://dx.doi.org/10.3390/ijms24043126.

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To determine the origin of oscillatory potentials (OPs), binocular electroretinogram (ERG) recordings were performed under light and dark adaptation on adult healthy C57BL/6J mice. In the experimental group, 1 μL of PBS was injected into the left eye, while the right eye was injected with 1 μL of PBS containing different agents: APB, GABA, Bicuculline, TPMPA, Glutamate, DNQX, Glycine, Strychnine, or HEPES. The OP response depends on the type of photoreceptors involved, showing their maximum response amplitude in the ERG induced by mixed rod/cone stimulation. The oscillatory components of the O
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Sethuramanujam, Santhosh, and Malcolm M. Slaughter. "Disinhibitory recruitment of NMDA receptor pathways in retina." Journal of Neurophysiology 112, no. 1 (2014): 193–203. http://dx.doi.org/10.1152/jn.00817.2013.

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Glutamate release at bipolar to ganglion cell synapses activates NMDA and AMPA/kainic acid (KA) ionotropic glutamate receptors. Their relative strength determines the output signals of the retina. We found that this balance is tightly regulated by presynaptic inhibition that preferentially suppresses NMDA receptor (NMDAR) activation. In transient ON-OFF neurons, block of GABA and glycine feedback enhanced total NMDAR charge by 35-fold in the ON response and 9-fold in the OFF compared with a 1.7-fold enhancement of AMPA/KA receptors. Blocking only glycine receptors enhanced the NMDAR excitatory
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Yamamoto, Ryo, Takafumi Furuyama, Tokio Sugai, Munenori Ono, Denis Pare, and Nobuo Kato. "Serotonergic control of GABAergic inhibition in the lateral amygdala." Journal of Neurophysiology 123, no. 2 (2020): 670–81. http://dx.doi.org/10.1152/jn.00500.2019.

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Much evidence implicates the serotonergic regulation of the amygdala in anxiety. Thus the present study was undertaken to characterize the influence of serotonin (5-HT) on principal neurons (PNs) of the rat lateral amygdala (LA), using whole cell recordings in vitro. Because inhibition is a major determinant of PN activity, we focused on the control of GABAergic transmission by 5-HT. IPSCs were elicited by local electrical stimulation of LA in the presence of glutamate receptor antagonists. We found that 5-HT reduces GABAA inhibitory postsynaptic currents (IPSCs) via presynaptic 5-HT1B recepto
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Nurullin, L. F., N. D. Almazov, and E. M. Volkov. "Immunofluorescent Identification of GABAergic Structures in the Somatic Muscle of the Earthworm <i>Lumbricus terrestris</i>." Биологические мембраны Журнал мембранной и клеточной биологии 40, no. 6 (2023): 449–55. http://dx.doi.org/10.31857/s0233475523060075.

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Using the immunofluorescence confocal microscopy, we detected the following GABAergic structures in the somatic muscle of the body wall of the earthworm: neurotransmitter gamma-aminobutyric acid (GABA); the enzyme responsible for synthesis of GABA, glutamate decarboxylase; type 1, 2, and 3 membrane transporters of GABA providing its reuptake; pre- and postsynaptic type A (ionotropic) and type B (metabotropic) GABA receptors. These structures are localized in the areas of cholinergic neuromuscular synapses. We assume that GABA can participate in modulation of motor activity of the earthworm som
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Chéry, Nadège, and 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 (2000): 1006–11. http://dx.doi.org/10.1152/jn.2000.84.2.1006.

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We have previously provided functional evidence that glycine and GABA are contained in the same synaptic vesicles and coreleased at the same synapses in lamina I of the rat spinal dorsal horn. However, whereas both glycine receptors (GlyRs) and GABAA receptors (GABAARs) are expressed on the postsynaptic target, under certain conditions inhibitory events appeared to be mediated by GlyRs only. We therefore wanted to test whether GABAB receptors could be activated in conditions where GABA released was insufficient to activate GABAARs. Focal stimulation in the vicinity of visually identified lamin
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Dissertations / Theses on the topic "GABA, glutamate,synapses"

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Pizzarelli, Rocco. "Trans-synaptic signaling at GABAergic connections: possible dysfunction in some forms of Autism Spectrum Disorders." Doctoral thesis, SISSA, 2012. http://hdl.handle.net/20.500.11767/4721.

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Synapses are recognized as being highly plastic in structure and function, strongly influenced by their own histories of impulse traffic and by signals from nearby cells. Synaptic contacts are fundamental for the development, homeostasis and remodeling of complex neural circuits. Synapses are highly varied in their molecular composition. Understand this diversity is important because it sheds light on the way they function. In particular, this may be useful for understanding the mechanisms at the basis of synaptic dysfunctions associated with neurodevelopmental disorders, such as Autism Spectr
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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.

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Pin, 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.

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Boulland, 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.

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El, 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.

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MeCP2 est une protéine multifonctionnelle agissant à de nombreux niveaux de contrôle des programmes génétiques. Un mauvais dosage de MeCP2 cause un groupe de maladies neurologiques dont le point commun est une déficience intellectuelle sévère. Des mutations ou une délétion de MECP2 causent le syndrome de Rett chez les filles, alors que sa surexpression cause chez les garçons le syndrome de duplication de MECP2. Plusieurs modèles murins de Mecp2-pathies ont été générés qui permettent d’expliciter les mécanismes qui sous-tendent l’apparition des symptômes dans ces différentes maladies. Dans notr
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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.

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Piot, 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.

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Les récepteurs ionotropiques du glutamate (iGluRs) sont les principaux médiateurs de la transmission excitatrice dans le système nerveux central (SNC) des Vertébrés. Il a longtemps été considéré que les réponses biologiques provoquées par les iGluRs étaient nécessairement liées au flux d’ions à travers leur canal, d’où l’appellation « ionotropique ». Toutefois de nombreuses données indiquent que plusieurs membres de cette classe de récepteurs peuvent provoquer des signalisations intracellulaires sans ouverture de leur canal. C’est le cas des récepteurs delta, classe comprenant deux membres (Gl
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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.

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Les récepteurs métabotropiques du glutamate (mGluRs) sont des récepteurs couplés aux protéines G (RCPGs) modulant la transmission synaptique au sein du système nerveux central. D'un point de vue structural, ils ont la particularité de posséder un large domaine extracellulaire, le Venus Flytrap (VFT), où se lie leur ligand endogène, le glutamate. Leur domaine transmembranaire à 7 hélices, commun à tous les RCPGs, est connu pour être la cible d'une nouvelle classe de molécules à visée thérapeutique, les modulateurs allostériques. Au contraire, le VFT est le siège du développement de ligands comp
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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.

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Book chapters on the topic "GABA, glutamate,synapses"

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Gillespie, Deda C., and Karl Kandler. "GABA, Glycine, and Glutamate Co-Release at Developing Inhibitory Synapses." In Co-Existence and Co-Release of Classical Neurotransmitters. Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-09622-3_5.

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Pin, Jean-Philippe, and Joël Bockaert. "Metabotropic glutamate receptors." In Understanding G protein-coupled receptors and their role in the CNS. Oxford University PressOxford, 2002. http://dx.doi.org/10.1093/oso/9780198509165.003.0029.

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Abstract Glutamate, like other neurotransmitters (acetylcholine, ATP, serotonine, glycine, GABA), acts on two main types of membrane receptors: ligand-gated channels, also called ionotropic receptors (iGluRs), and G protein coupled receptors also called metabotropic glutamate receptors (mGluRs). In contrast to the iGluRs that are primarily responsible for the fast excitatory synaptic transmission, mGluRs are generally involved in the tuning not only of glutamatergic synapses, but also GABA-ergic, dopaminergic and serotoninergic synapses. As such these receptors represent an excellent target fo
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Perry, Elaine, Rose Goodchild, and Margaret Piggott. "Neurochemical pathology in degenerative dementias." In Early-Onset Dementia: a multidisciplinary approach. Oxford University PressNew York, NY, 2001. http://dx.doi.org/10.1093/oso/9780192630346.003.0009.

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Abstract The focus of this chapter on transmitter abnormalities in dementia is: how transmitter deficits contribute to cognitive and non-cognitive/neuropsychiatric clinical features; how these can be targeted by specific pharmacotherapies; and, if such therapies are of clinical value, whether diagnostic markers of relevant transmitter disturbances (such as in vivo neuroimaging) can be developed to facilitate disease management. Chemical messengers involved in CNS signalling can be divided into two groups. There are neurotransmitters, released at synapses that operate via ionotropic receptors,
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Maynard, R. A., and T. C. Marrs. "Introduction." In Neurotransmitters and Toxicology. Royal Society of Chemistry, 2024. http://dx.doi.org/10.1039/9781839165795-00001.

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Neurotransmission systems exist in all multicellular animals and enable inter-neuronal transmission at synapses and from nerve cells to effector organs such as skeletal muscles and glands. They are complex, comprising afferent nerves, containing the neurotransmitter, where it is synthesized and stored in vesicles, from which the transmitter is released in response to a nerve impulse. At the synapse, neuromuscular junction and autonomic effector organs, there are specialized receptors where binding of the neurotransmitter induces a response. There are many different neurotransmitters, including
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