Relevant bibliographies by topics / Metabotropic Glutamate Synapses Synapses Synaptic Transmission

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

Academic literature on the topic 'Metabotropic Glutamate Synapses Synapses Synaptic Transmission'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 February 2022

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Journal articles on the topic "Metabotropic Glutamate Synapses Synapses Synaptic Transmission"

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Robberechts, Quinten, Mike Wijnants, Michele Giugliano, and Erik De Schutter. "Long-Term Depression at Parallel Fiber to Golgi Cell Synapses." Journal of Neurophysiology 104, no. 6 (2010): 3413–23. http://dx.doi.org/10.1152/jn.00030.2010.

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Golgi cells (GoCs) are the primary inhibitory interneurons of the granular layer of the cerebellum. Their inhibition of granule cells is central to operate the relay of excitatory inputs to the cerebellar cortex. Parallel fibers (PFs) establish synapses to the GoCs in the molecular layer; these synapses contain AMPA, N-methyl-d-aspartate (NMDA), and mostly group II metabotropic glutamate receptors. Long-term changes in the efficacy of synaptic transmission at the PF-GoC synapse have not been described previously. We used whole cell patch-clamp recordings of GoCs in acute rat cerebellar slices
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Abrahamsson, Therése, Bengt Gustafsson, and Eric Hanse. "Reversible Synaptic Depression in Developing Rat CA3–CA1 Synapses Explained by a Novel Cycle of AMPA Silencing-Unsilencing." Journal of Neurophysiology 98, no. 5 (2007): 2604–11. http://dx.doi.org/10.1152/jn.00602.2007.

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In the developing hippocampus, experiments using whole cell recordings have shown that a small number of synaptic activations can convert many glutamate synapses to AMPA silent synapses. This depression of AMPA signaling is induced by low-frequency (0.05–0.2 Hz) activation, does not require N-methyl-d-aspartate or metabotropic glutamate receptor activation for its induction, and does not readily reverse after stimulus interruption. Here we show, using field recordings and perforated patch-clamp recordings of transmission in developing CA3–CA1 synapses, that this synaptic depression also can be
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Xiang, Zixiu, Xiaohui Lv, Xin Lin, et al. "Input-specific regulation of glutamatergic synaptic transmission in the medial prefrontal cortex by mGlu2/mGlu4 receptor heterodimers." Science Signaling 14, no. 677 (2021): eabd2319. http://dx.doi.org/10.1126/scisignal.abd2319.

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Metabotropic glutamate receptors (mGluRs) are G protein–coupled receptors that regulate various aspects of central nervous system processing in normal physiology and in disease. They are thought to function as disulfide-linked homodimers, but studies have suggested that mGluRs can form functional heterodimers in cell lines. Using selective allosteric ligands, ex vivo brain slice electrophysiology, and optogenetic approaches, we found that two mGluR subtypes—mGluR2 and mGluR4 (or mGlu2 and mGlu4)—exist as functional heterodimers that regulate excitatory transmission in a synapse-specific manner
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Alexander, Georgia M., and Dwayne W. Godwin. "Presynaptic Inhibition of Corticothalamic Feedback by Metabotropic Glutamate Receptors." Journal of Neurophysiology 94, no. 1 (2005): 163–75. http://dx.doi.org/10.1152/jn.01198.2004.

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The thalamus relays sensory information to cortex, but this information may be influenced by excitatory feedback from cortical layer VI. The full importance of this feedback has only recently been explored, but among its possible functions are influences on the processing of sensory features, synchronization of thalamic firing, and transitions in response mode of thalamic relay cells. Uncontrolled, corticothalamic feedback has also been implicated in pathological thalamic rhythms associated with certain neurological disorders. We have found a form of presynaptic inhibition of corticothalamic s
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Liu, Yan, Shan Wang, Jun Kan, et al. "Chinese Herbal Medicine Interventions in Neurological Disorder Therapeutics by Regulating Glutamate Signaling." Current Neuropharmacology 18, no. 4 (2020): 260–76. http://dx.doi.org/10.2174/1570159x17666191101125530.

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Glutamate is the major excitatory neurotransmitter in the central nervous system, and its signaling is critical for excitatory synaptic transmission. The well-established glutamate system involves glutamate synthesis, presynaptic glutamate release, glutamate actions on the ionotropic glutamate receptors (NMDA, AMPA, and kainate receptors) and metabotropic glutamate receptors, and glutamate uptake by glutamate transporters. When the glutamate system becomes dysfunctional, it contributes to the pathogenesis of neurodegenerative and neuropsychiatric diseases such as Alzheimer's disease,
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Doherty, James, and Raymond Dingledine. "Differential Regulation of Synaptic Inputs to Dentate Hilar Border Interneurons by Metabotropic Glutamate Receptors." Journal of Neurophysiology 79, no. 6 (1998): 2903–10. http://dx.doi.org/10.1152/jn.1998.79.6.2903.

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Doherty, James and Raymond Dingledine. Differential regulation of synaptic inputs to dentate hilar border interneurons by metabotropic glutamate receptors. J. Neurophysiol. 79: 2903–2910, 1998. Regulation of synaptic transmission by metabotropic glutamate receptors (mGluRs) was examined at two excitatory inputs to interneurons with cell bodies at the granule cell–hilus border in hippocampal slices taken from neonatal rats. Subgroup-selective mGluR agonists altered the reliability, or probability of transmitter release, of evoked minimal excitatory synaptic inputs and decreased the amplitudes o
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Huang, Yixian, Haiyang Shu, Li Li, et al. "L-DOPA-Induced Motor Impairment and Overexpression of Corticostriatal Synaptic Components Are Improved by the mGluR5 Antagonist MPEP in 6-OHDA-Lesioned Rats." ASN Neuro 10 (January 2018): 175909141881102. http://dx.doi.org/10.1177/1759091418811021.

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Levodopa (L-DOPA) is still the most effective drug for the treatment of Parkinson’s disease (PD). However, the long-term therapy often triggers L-DOPA-induced dyskinesia (LID). Metabotropic glutamate receptor type 5 (mGluR5) is abundant in the basal ganglia, and its inhibition is thought to modulate postsynaptic excitatory synaptic transmission and glutamate hyperactivity in PD and LID. In this report, we examined the effects of mGluR5-specific antagonist 2-methyl-6-(phenylethynyl)pyridine (MPEP) on LID and synaptic components in the PD model rat. We found the selective mGluR5 antagonist MPEP
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Lovinger, D. M., and B. A. McCool. "Metabotropic glutamate receptor-mediated presynaptic depression at corticostriatal synapses involves mGLuR2 or 3." Journal of Neurophysiology 73, no. 3 (1995): 1076–83. http://dx.doi.org/10.1152/jn.1995.73.3.1076.

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1. The pharmacology of the metabotropic glutamate receptor (mGluR) that mediates synaptic depression at corticostriatal synapses was investigated with the use of field potential and whole cell patch-clamp recording from striatal slices and whole cell recordings from isolated striatal neurons. 2. The mGluR2,3-selective agonists (R,S)-4-carboxy-3-hydroxyphenylglycine (CHPG), (2S, 1'R,2'R,3'R)-2-(2,3-dicarboxycyclopropyl) glycine (DCG-IV), and (2S, 3S, 4S)-alpha-(carboxycyclopropyl) glycine (L-CCG-I) inhibited the synaptically driven population spike (PS) evoked by afferent stimulation during fie
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Karakossian, Movses H., and Thomas S. Otis. "Excitation of Cerebellar Interneurons by Group I Metabotropic Glutamate Receptors." Journal of Neurophysiology 92, no. 3 (2004): 1558–65. http://dx.doi.org/10.1152/jn.00300.2004.

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Cerebellar basket and stellate neurons (BSNs) provide feed-forward inhibition to Purkinje neurons (PNs) and thereby play a principal role in determining the output of the cerebellar cortex. During low-frequency transmission, glutamate released at parallel fiber synapses excites BSNs by binding to AMPA receptors; high-frequency transmission also recruits N-methyl-d-aspartate (NMDA) receptors. We find that, in addition to these ligand-gated receptors, a G-protein–coupled glutamate receptor subtype participates in exciting BSNs. Stimulation of metabotropic glutamate receptor 1α (mGluR1α) with the
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Lovinger, D. M., E. Tyler, S. Fidler, and A. Merritt. "Properties of a presynaptic metabotropic glutamate receptor in rat neostriatal slices." Journal of Neurophysiology 69, no. 4 (1993): 1236–44. http://dx.doi.org/10.1152/jn.1993.69.4.1236.

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1. The effect of the metabotropic glutamate receptor agonist trans-1-aminocyclopentane-1,3-dicarboxylic acid (t-ACPD) on glutamatergic transmission at corticostriate synapses was examined using slices of neostriatum. Field potential recordings were performed in slices from adult animals, and the effects of t-ACPD on the synaptically driven population spike were examined. Tight-seal whole-cell recordings were made in slices from 2 to 4-wk-old rats, and effects of t-ACPD on the amplitude of excitatory postsynaptic potentials (EPSPs) and postsynaptic neuronal membrane properties were examined. In
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Dissertations / Theses on the topic "Metabotropic Glutamate Synapses Synapses Synaptic Transmission"

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Speed, Haley E. "Changes in short-term facilitation are opposite at Schaffer collateral and Temporoammonic CA1 synapses in the developing rat hippocampus." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2008p/speed.pdf.

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Tassin, Valériane. "Nouveaux mécanismes d'action du récepteur mGlu7a dans le thalamus : de la synapse au comportement." Thesis, Montpellier 1, 2014. http://www.theses.fr/2014MON13509/document.

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Le fonctionnement cérébral est régit par deux grandes forces : un système excitateur, principalement supporté par la transmission gluue,tamatergiq qui s'oppose à un système inhibiteur, principalement supporté par la transmission GABAergique. L'influence mutuelle et équilibrée de ces deux forces est déterminante pour établir et maintenir une activité neuronale physiologique au sein des réseaux neuronaux. Le récepteur métabotropique du glutamate de type 7, mGlu7, est capable de moduler à la fois la transmission glutamatergique et GABAergique, mais sa localisation et son rôle synaptique précis re
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Hauser, Jessica Lauren. "Mechanisms Shaping Excitatory Transmission at the Developing Retinogeniculate Synapse." Thesis, Harvard University, 2014. http://nrs.harvard.edu/urn-3:HUL.InstRepos:13090521.

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The retinogeniculate synapse, the connection between retinal ganglion cells (RGCs) and thalamic relay neurons, undergoes extensive remodeling and refinement in the first few postnatal weeks. While many studies have focused on this process, little is known about the factors that influence excitatory transmission during this dynamic period. A major goal of my dissertation research was to identify mechanisms that regulate glutamate release and clearance at the developing synapse. First, we investigated the role of glutamate transporters and metabotropic glutamate receptors (mGluRs) in shaping exc
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Ayman, Göher. "Dynamic aspects of the control of excitatory transmission by metabotropic glutamate receptors at cortical synapses of rat brain." Thesis, University of Bristol, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414358.

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Sims-Robinson, Catrina Suppiramaniam Vishnu. "Differential modulation of glutamatergic synaptic transmission by polysialic acid." Auburn, Ala, 2007. http://hdl.handle.net/10415/1352.

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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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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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Book chapters on the topic "Metabotropic Glutamate Synapses Synapses Synaptic Transmission"

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Benarroch, Eduardo E. "Glutamatergic Transmission and Synaptopathies." In Neuroscience for Clinicians, edited by Eduardo E. Benarroch. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.003.0017.

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L-glutamate is the primary excitatory neurotransmitter in the adult central nervous system (CNS). Glutamatergic inputs are critical for fast synaptic excitation, use-dependent synaptic plasticity, shaping of activity of local circuits and networks, neuron–astrocyte interactions, and myelination by oligodendrocytes. Plasticity of glutamatergic synapses is critical for development and maintenance of synaptic connections and for mechanisms of learning and adaptation in the CNS. Induction of these forms of glutamatergic synaptic plasticity depends on the activity-dependent expression and recycling of glutamate receptor subunits. Impaired plasticity of glutamatergic synapses is a major disease mechanism in neurodevelopmental intellectual disability, Alzheimer disease, limbic encephalitis, and cerebellar ataxia.
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