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

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1

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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2

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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3

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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4

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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5

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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6

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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8

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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9

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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10

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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11

Sidorov, Michael S., Eitan S. Kaplan, Emily K. Osterweil, Lothar Lindemann, and Mark F. Bear. "Metabotropic glutamate receptor signaling is required for NMDA receptor-dependent ocular dominance plasticity and LTD in visual cortex." Proceedings of the National Academy of Sciences 112, no. 41 (2015): 12852–57. http://dx.doi.org/10.1073/pnas.1512878112.

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A feature of early postnatal neocortical development is a transient peak in signaling via metabotropic glutamate receptor 5 (mGluR5). In visual cortex, this change coincides with increased sensitivity of excitatory synapses to monocular deprivation (MD). However, loss of visual responsiveness after MD occurs via mechanisms revealed by the study of long-term depression (LTD) of synaptic transmission, which in layer 4 is induced by acute activation of NMDA receptors (NMDARs) rather than mGluR5. Here we report that chronic postnatal down-regulation of mGluR5 signaling produces coordinated impairm
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Creed, Meaghan, Vincent Jean Pascoli, and Christian Lüscher. "Refining deep brain stimulation to emulate optogenetic treatment of synaptic pathology." Science 347, no. 6222 (2015): 659–64. http://dx.doi.org/10.1126/science.1260776.

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Circuit remodeling driven by pathological forms of synaptic plasticity underlies several psychiatric diseases, including addiction. Deep brain stimulation (DBS) has been applied to treat a number of neurological and psychiatric conditions, although its effects are transient and mediated by largely unknown mechanisms. Recently, optogenetic protocols that restore normal transmission at identified synapses in mice have provided proof of the idea that cocaine-adaptive behavior can be reversed in vivo. The most efficient protocol relies on the activation of metabotropic glutamate receptors, mGluRs,
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13

Watabe, Ayako M., Holly J. Carlisle, and Thomas J. O'Dell. "Postsynaptic Induction and Presynaptic Expression of Group 1 mGluR-Dependent LTD in the Hippocampal CA1 Region." Journal of Neurophysiology 87, no. 3 (2002): 1395–403. http://dx.doi.org/10.1152/jn.00723.2001.

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Activation of metabotropic glutamate receptors (mGluRs) with the group I mGluR selective agonist (R,S)-3,5-dihydroxyphenylglycine (DHPG) induces a long-term depression (LTD) of excitatory synaptic transmission in the CA1 region of the hippocampus. Here we investigated the potential roles of pre- and postsynaptic processes in the DHPG-induced LTD at excitatory synapses onto hippocampal pyramidal cells in the mouse hippocampus. Activation of mGluRs with DHPG, but not ACPD, induced LTD at both Schaffer collateral/commissural fiber synapses onto CA1 pyramidal cells and at associational/commissural
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Mitoma, Hiroshi, Jerome Honnorat, Kazuhiko Yamaguchi, and Mario Manto. "Fundamental Mechanisms of Autoantibody-Induced Impairments on Ion Channels and Synapses in Immune-Mediated Cerebellar Ataxias." International Journal of Molecular Sciences 21, no. 14 (2020): 4936. http://dx.doi.org/10.3390/ijms21144936.

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In the last years, different kinds of limbic encephalitis associated with autoantibodies against ion channels and synaptic receptors have been described. Many studies have demonstrated that such autoantibodies induce channel or receptor dysfunction. The same mechanism is discussed in immune-mediated cerebellar ataxias (IMCAs), but the pathogenesis has been less investigated. The aim of the present review is to evaluate what kind of cerebellar ion channels, their related proteins, and the synaptic machinery proteins that are preferably impaired by autoantibodies so as to develop cerebellar atax
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15

Sanchez-Pernaute, Rosario, and Anna-Liisa Brownell. "Therapeutic Exploration of Metabotropic Glutamate Receptor Antagonists in Parkinson’s Disease by Positron Emission Tomography." US Neurology 05, no. 02 (2010): 21. http://dx.doi.org/10.17925/usn.2010.05.02.21.

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Metabotropic glutamate receptors (mGluR)s are G-protein-coupled receptors that function as modulators of synaptic function and glutamate transmission. Post-synaptically localized subtype 5 mGlu5 receptors are co-localized with adenosine A2a, dopamine, and N-methyl-D-aspartate (NMDA) receptors and regulate local protein synthesis and messenger RNA (mRNA) translation at synapses, and are thus ideally positioned to control synaptic plasticity. Aberrant synaptic plasticity appears to be involved in a number of developmental and degenerative neuropsychiatric disorders, including Parkinson’s disease
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LIU, QING-SONG, QIWU XU, JIAN KANG, and MAIKEN NEDERGAARD. "Astrocyte activation of presynaptic metabotropic glutamate receptors modulates hippocampal inhibitory synaptic transmission." Neuron Glia Biology 1, no. 4 (2004): 307–16. http://dx.doi.org/10.1017/s1740925x05000190.

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In the CNS, fine processes of astrocytes often wrap around dendrites, axons and synapses, which provides an interface where neurons and astrocytes might interact. We have reported previously that selective Ca2+ elevation in astrocytes, by photolysis of caged Ca2+ by o-nitrophenyl-EGTA (NP-EGTA), causes a kainite receptor-dependent increase in the frequency of spontaneous inhibitory post-synaptic potentials (sIPSCs) in neighboring interneurons in hippocampal slices. However, tetrodotoxin (TTX), which blocks action potentials, reduces the frequency of miniature IPSCs (mIPSCs) in interneurons dur
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17

HIGGS, MATTHEW H., and PETER D. LUKASIEWICZ. "Activation of group II metabotropic glutamate receptors inhibits glutamate release from salamander retinal photoreceptors." Visual Neuroscience 19, no. 3 (2002): 275–81. http://dx.doi.org/10.1017/s0952523802192054.

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We investigated the effects of group II metabotropic glutamate receptor (mGluR) activation on excitatory synaptic transmission in the salamander retinal slice preparation. The group II selective agonists DCG-IV and LY354740 reduced light-evoked excitatory postsynaptic currents (EPSCs) in ganglion cells. To determine the synaptic basis of this effect, we also recorded from bipolar cells and horizontal cells. In ON bipolar cells, DCG-IV increased the inward current in darkness but did not affect the peak current at light onset. In OFF bipolar cells and horizontal cells, DCG-IV had the opposite e
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18

Garrido Sanabria, Emilio R., Krystyna M. Wozniak, Barbara S. Slusher, and Asaf Keller. "GCP II (NAALADase) Inhibition Suppresses Mossy Fiber-CA3 Synaptic Neurotransmission by a Presynaptic Mechanism." Journal of Neurophysiology 91, no. 1 (2004): 182–93. http://dx.doi.org/10.1152/jn.00465.2003.

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We tested the hypothesis that endogenous N-acetylaspartylglutamate (NAAG) presynaptically inhibits glutamate release at mossy fiber-CA3 synapses. For this purpose, we made use of 2-(3-mercaptopropyl)pentanedioic acid (2-MPPA), an inhibitor of glutamate carboxypeptidase II [GCP II; also known as N-acetylated alpha-linked acidic dipeptidase (NAALADase)], the enzyme that hydrolyzes NAAG into N-acetylaspartate and glutamate. Application of 2-MPPA (1–20 μM) had no effect on intrinsic membrane properties of CA3 pyramidal neurons recorded in vitro in whole cell current- or voltage-clamp mode. Bath ap
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19

Belmeguenai, Amor, Paolo Botta, John T. Weber, et al. "Alcohol Impairs Long-Term Depression at the Cerebellar Parallel Fiber–Purkinje Cell Synapse." Journal of Neurophysiology 100, no. 6 (2008): 3167–74. http://dx.doi.org/10.1152/jn.90384.2008.

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Acute alcohol consumption causes deficits in motor coordination and gait, suggesting an involvement of cerebellar circuits, which play a role in the fine adjustment of movements and in motor learning. It has previously been shown that ethanol modulates inhibitory transmission in the cerebellum and affects synaptic transmission and plasticity at excitatory climbing fiber (CF) to Purkinje cell synapses. However, it has not been examined thus far how acute ethanol application affects long-term depression (LTD) and long-term potentiation (LTP) at excitatory parallel fiber (PF) to Purkinje cell syn
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Ireland, David R., and Wickliffe C. Abraham. "Mechanisms of Group I mGluR-Dependent Long-Term Depression of NMDA Receptor–Mediated Transmission at Schaffer Collateral–CA1 Synapses." Journal of Neurophysiology 101, no. 3 (2009): 1375–85. http://dx.doi.org/10.1152/jn.90643.2008.

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The mechanisms underlying group I metabotropic glutamate receptor (mGluR)-dependent long-term depression (LTD) of N-methyl-d-aspartate receptor (NMDAR)-mediated synaptic currents (EPSCsNMDAR) are poorly understood. Here we investigated the effects of ( R,S)-3,5-dihydroxyphenylglycine (DHPG), a selective agonist of group I mGluRs, on the EPSCsNMDAR in area CA1 of acute hippocampal slices from 6- to 8-wk Sprague-Dawley rats. DHPG acutely and persistently depressed the isolated EPSCNMDAR and transiently slowed its decay rate. Combined antagonism of mGluR1 and mGluR5 blocked the effects of DHPG. S
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Guntupalli, Sumasri, Jocelyn Widagdo та Victor Anggono. "Amyloid-β-Induced Dysregulation of AMPA Receptor Trafficking". Neural Plasticity 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/3204519.

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Evidence from neuropathological, genetic, animal model, and biochemical studies has indicated that the accumulation of amyloid-beta (Aβ) is associated with, and probably induces, profound neuronal changes in brain regions critical for memory and cognition in the development of Alzheimer’s disease (AD). There is considerable evidence that synapses are particularly vulnerable to AD, establishing synaptic dysfunction as one of the earliest events in pathogenesis, prior to neuronal loss. It is clear that excessive Aβlevels can disrupt excitatory synaptic transmission and plasticity, mainly due to
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22

Sung, Ki-Wug, Sukwoo Choi, and David M. Lovinger. "Activation of Group I mGluRs Is Necessary for Induction of Long-Term Depression at Striatal Synapses." Journal of Neurophysiology 86, no. 5 (2001): 2405–12. http://dx.doi.org/10.1152/jn.2001.86.5.2405.

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Activation of metabotropic glutamate receptors (mGluRs), which are coupled to G proteins, has important roles in certain forms of synaptic plasticity including corticostriatal long-term depression (LTD). In the present study, extracellular field potential and whole cell voltage-clamp recording techniques were used to investigate the effect of mGluR antagonists with different subtype specificity on high-frequency stimulation (HFS)-induced LTD of synaptic transmission in the striatum of brain slices obtained from 15-to 25-day-old rats. Induction of LTD was prevented during exposure to the nonsel
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23

Gipson, Keith E., and Mark F. Yeckel. "Coincident Glutamatergic and Cholinergic Inputs Transiently Depress Glutamate Release at Rat Schaffer Collateral Synapses." Journal of Neurophysiology 97, no. 6 (2007): 4108–19. http://dx.doi.org/10.1152/jn.01051.2006.

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The mammalian hippocampus, together with subcortical and cortical areas, is responsible for some forms of learning and memory. Proper hippocampal function depends on the highly dynamic nature of its circuitry, including the ability of synapses to change their strength for brief to long periods of time. In this study, we focused on a transient depression of glutamatergic synaptic transmission at Schaffer collateral synapses in acute hippocampal slices. The depression of evoked excitatory postsynaptic current (EPSC) amplitudes, herein called transient depression, follows brief trains of synaptic
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24

Crépel, Francis. "Role of Presynaptic Kainate Receptors at Parallel Fiber–Purkinje Cell Synapses in Induction of Cerebellar LTD: Interplay With Climbing Fiber Input." Journal of Neurophysiology 102, no. 2 (2009): 965–73. http://dx.doi.org/10.1152/jn.00269.2009.

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Until recently, except for A1 adenosine, N-methyl-d-aspartate, and cannabinoid receptors, little effort has been made to unravel possible roles of parallel fiber (PF) presynaptic receptors in long-term depression (LTD) of synaptic transmission at PF–Purkinje cell (PC) synapses. Presynaptic kainate (KA) receptors are also present on PFs and might also influence LTD induction by modulating glutamate (Glu) release at PF–PC synapses. This hypothesis was tested by comparing the efficacy of two pairing protocols in inducing LTD in adult wild-type and knock-out mice for the Glu receptor 6 (GluR6) sub
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Sekizawa, Shin-ichi, and Ann C. Bonham. "Group I Metabotropic Glutamate Receptors on Second-Order Baroreceptor Neurons Are Tonically Activated and Induce a Na+–Ca2+ Exchange Current." Journal of Neurophysiology 95, no. 2 (2006): 882–92. http://dx.doi.org/10.1152/jn.00772.2005.

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The nucleus tractus solitarius (NTS) is essential for coordinating baroreflex control of blood pressure. The baroreceptor sensory fibers make glutamatergic synapses onto second-order NTS neurons. Glutamate spillover activates Group II and III presynaptic metabotropic glutamate receptors (mGluRs) on the baroreceptor central terminals to inhibit synaptic transmission, but the role of postsynaptic mGluRs is less understood. We used whole cell patch-clamping in anatomically identified second-order baroreceptor neurons in a brain stem slice to test whether Group I, II, and III mGluRs had postsynapt
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Martín, Ricardo, José Javier Ferrero, Andrea Collado-Alsina, et al. "Bidirectional modulation of glutamatergic synaptic transmission by metabotropic glutamate type 7 receptors at Schaffer collateral-CA1 hippocampal synapses." Journal of Physiology 596, no. 5 (2018): 921–40. http://dx.doi.org/10.1113/jp275371.

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Olivero, Guendalina, Matteo Vergassola, Francesca Cisani, Alessandra Roggeri, and Anna Pittaluga. "Presynaptic Release-regulating Metabotropic Glutamate Receptors: An Update." Current Neuropharmacology 18, no. 7 (2020): 655–72. http://dx.doi.org/10.2174/1570159x17666191127112339.

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: Metabotropic glutamate (mGlu) receptors represent the largest family of glutamate receptors in mammals and act as fine tuners of the chemical transmission in central nervous system (CNS). : In the last decade, results concerning the expression and the subcellular localization of mGlu receptors further clarified their role in physio-pathological conditions. Concomitantly, their pharmacological characterization largely improved thanks to the identification of new compounds (chemical ligands and antibodies recognizing epitopic sequences of the receptor proteins) that allowed to decipher the pro
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Jo, J., S. Heon, M. J. Kim, et al. "Metabotropic Glutamate Receptor-mediated LTD Involves two Interacting Ca2+ Sensors, NCS-1 and PICK1." European Psychiatry 24, S1 (2009): 1. http://dx.doi.org/10.1016/s0924-9338(09)70317-7.

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There are two major forms of long-term depression (LTD) of synaptic transmission in the central nervous system, which require activation of either N-methyl-D-aspartate receptors (NMDARs) or metabotropic glutamate receptors (mGluRs). In synapses in the perirhinal cortex we have directly compared the Ca2+ signalling mechanisms involved in NMDAR-LTD and mGluR-LTD. Whilst both forms of LTD involve Ca2+ release from intracellular stores the Ca2+ sensors involved are different; NMDAR-LTD involves calmodulin, whilst mGluR-LTD involves the neuronal Ca2+ sensor (NCS) protein NCS-1. In addition, there i
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D'Angelo, Egidio, Paola Rossi, Simona Armano, and Vanni Taglietti. "Evidence for NMDA and mGlu Receptor-Dependent Long-Term Potentiation of Mossy Fiber–Granule Cell Transmission in Rat Cerebellum." Journal of Neurophysiology 81, no. 1 (1999): 277–87. http://dx.doi.org/10.1152/jn.1999.81.1.277.

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D'Angelo, Egidio, Paola Rossi, Simona Armano, and Vanni Taglietti. Evidence for NMDA and mGlu receptor-dependent long-term potentiation of mossy fiber–granule cell transmission in rat cerebellum. J. Neurophysiol. 81: 277–287, 1999. Long-term potentiation (LTP) is a form of synaptic plasticity that can be revealed at numerous hippocampal and neocortical synapses following high-frequency activation of N-methyl-d-aspartate (NMDA) receptors. However, it was not known whether LTP could be induced at the mossy fiber–granule cell relay of cerebellum. This is a particularly interesting issue because t
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Loerwald, Kristofer W., Ankur B. Patel, Kimberly M. Huber, and Jay R. Gibson. "Postsynaptic mGluR5 promotes evoked AMPAR-mediated synaptic transmission onto neocortical layer 2/3 pyramidal neurons during development." Journal of Neurophysiology 113, no. 3 (2015): 786–95. http://dx.doi.org/10.1152/jn.00465.2014.

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Both short- and long-term roles for the group I metabotropic glutamate receptor number 5 (mGluR5) have been examined for the regulation of cortical glutamatergic synapses. However, how mGluR5 sculpts neocortical networks during development still remains unclear. Using a single cell deletion strategy, we examined how mGluR5 regulates glutamatergic synaptic pathways in neocortical layer 2/3 (L2/3) during development. Electrophysiological measurements were made in acutely prepared slices to obtain a functional understanding of the effects stemming from loss of mGluR5 in vivo. Loss of postsynaptic
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Schubert, Vanessa, Jorge Santos Da Silva, and Carlos G. Dotti. "Localized recruitment and activation of RhoA underlies dendritic spine morphology in a glutamate receptor–dependent manner." Journal of Cell Biology 172, no. 3 (2006): 453–67. http://dx.doi.org/10.1083/jcb.200506136.

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Actin is the major cytoskeletal source of dendritic spines, which are highly specialized protuberances on the neuronal surface where excitatory synaptic transmission occurs (Harris, K.M., and S.B. Kater. 1994. Annu. Rev. Neurosci. 17:341–371; Yuste, R., and D.W. Tank. 1996. Neuron. 16:701–716). Stimulation of excitatory synapses induces changes in spine shape via localized rearrangements of the actin cytoskeleton (Matus, A. 2000. Science. 290:754–758; Nagerl, U.V., N. Eberhorn, S.B. Cambridge, and T. Bonhoeffer. 2004. Neuron. 44:759–767). However, what remains elusive are the precise molecular
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Thompson, John A., and David J. Perkel. "Endocannabinoids mediate synaptic plasticity at glutamatergic synapses on spiny neurons within a basal ganglia nucleus necessary for song learning." Journal of Neurophysiology 105, no. 3 (2011): 1159–69. http://dx.doi.org/10.1152/jn.00676.2010.

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Activation of type 1 cannabinoid receptors (CB1R) in many central nervous system structures induces both short- and long-term changes in synaptic transmission. Within mammalian striatum, endocannabinoids (eCB) are one of several mechanisms that induce synaptic plasticity at glutamatergic terminals onto medium spiny neurons. Striatal synaptic plasticity may contribute a critical component of adaptive motor coordination and procedural learning. Songbirds are advantageous for studying the neural mechanisms of motor learning because they possess a neural pathway necessary for song learning and adu
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Molitor, Scott C., and Paul B. Manis. "Evidence for Functional Metabotropic Glutamate Receptors in the Dorsal Cochlear Nucleus." Journal of Neurophysiology 77, no. 4 (1997): 1889–905. http://dx.doi.org/10.1152/jn.1997.77.4.1889.

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Molitor, Scott C. and Paul B. Manis. Evidence for functional metabotropic glutamate receptors in the dorsal cochlear nucleus. J. Neurophysiol. 77: 1889–1905, 1997. The parallel fibers (PFs) of the dorsal cochlear nucleus (DCN) molecular layer use glutamate as a neurotransmitter. Although metabotropic glutamate receptors (mGluRs) have been identified on cells postsynaptic to the PFs, little is known about the effects of mGluR activation in PF synaptic transmission in the DCN. To investigate these effects, PF-evoked field potentials were recorded from the DCN in guinea pig brain stem slice prepa
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Giustizieri, Michela, Giorgio Bernardi, Nicola B. Mercuri, and Nicola Berretta. "Distinct Mechanisms of Presynaptic Inhibition at GABAergic Synapses of the Rat Substantia Nigra Pars Compacta." Journal of Neurophysiology 94, no. 3 (2005): 1992–2003. http://dx.doi.org/10.1152/jn.00171.2005.

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We investigated the mechanisms of presynaptic inhibition of GABAergic neurotransmission by group III metabotropic glutamate receptors (mGluRs) and GABAB receptors, in dopamine (DA) neurons of the substantia nigra pars compacta (SNc). Both the group III mGluRs agonist l-(+)-2-amino-4-phosphonobutyric acid (AP4, 100 μM) and the GABAB receptor agonist baclofen (10 μM) reversibly depressed the frequency of spontaneous inhibitory postsynaptic currents (sIPSCs) to 48.5 ± 2.7 and 79.3 ± 1.6% (means ± SE) of control, respectively. On the contrary, the frequency of action potential-independent miniatur
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Schrader, Laura A., Stephen P. Perrett, Lan Ye, and Michael J. Friedlander. "Substrates for Coincidence Detection and Calcium Signaling for Induction of Synaptic Potentiation in the Neonatal Visual Cortex." Journal of Neurophysiology 91, no. 6 (2004): 2747–64. http://dx.doi.org/10.1152/jn.00908.2003.

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Regulation of the efficacy of synaptic transmission by activity-dependent processes has been implicated in learning and memory as well as in developmental processes. We previously described transient potentiation of excitatory synapses onto layer 2/3 pyramidal neurons in the visual cortex that is induced by coincident presynaptic stimulation and postsynaptic depolarization. In the adult visual cortex, activation of N-methyl-d-aspartate (NMDA) glutamate receptors is necessary to induce this plasticity. These receptors act as coincidence detectors, sensing presynaptic glutamate release and posts
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Smart, Kelly, Atsuko Nagano-Saito, Michele S. Milella, et al. "Metabotropic glutamate type 5 receptor binding availability during dextroamphetamine sensitization in mice and humans." Journal of Psychiatry & Neuroscience 46, no. 1 (2020): E1—E13. http://dx.doi.org/10.1503/jpn.190162.

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Background: Glutamate transmission is implicated in drug-induced behavioural sensitization and the associated long-lasting increases in mesolimbic output. Metabotropic glutamate type 5 (mGlu5) receptors might be particularly important, but most details are poorly understood. Methods: We first assessed in mice (n = 51, all male) the effects of repeated dextroamphetamine administration (2.0 mg/kg, i.p.) on locomotor activity and binding of the mGlu5 ligand [3H]ABP688. In a parallel study, in 19 stimulant-drug-naïve healthy human volunteers (14 female) we administered 3 doses of dextroamphetamine
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Ouardouz, M., and J. C. Lacaille. "Mechanisms of selective long-term potentiation of excitatory synapses in stratum oriens/alveus interneurons of rat hippocampal slices." Journal of Neurophysiology 73, no. 2 (1995): 810–19. http://dx.doi.org/10.1152/jn.1995.73.2.810.

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1. We investigated long-term potentiation (LTP) of synaptic transmission in different populations of interneurons in the CA1 region of rat hippocampal slices using whole cell recordings. We elicited excitatory postsynaptic currents (EPSCs) in interneurons located in stratum oriens near the alveus (O/A) or in stratum lacunosum-moleculare near the stratum radiatum border (L-M) by electrical stimulation of nearby axons in stratum oriens and radiatum, respectively. 2. High-frequency stimulation (100 Hz, 1 s) of axons in conjunction with postsynaptic depolarization (to -20 mV) increased the peak am
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Maffei, Arianna, Francesca Prestori, Paola Rossi, Vanni Taglietti, and Egidio D'Angelo. "Presynaptic Current Changes at the Mossy Fiber–Granule Cell Synapse of Cerebellum During LTP." Journal of Neurophysiology 88, no. 2 (2002): 627–38. http://dx.doi.org/10.1152/jn.2002.88.2.627.

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The involvement of presynaptic mechanisms in the expression of long-term potentiation (LTP), an enhancement of synaptic transmission suggested to take part in learning and memory in the mammalian brain, has not been fully clarified. Although evidence for enhanced vesicle cycling has been reported, it is unknown whether presynaptic terminal excitability could change as has been observed in invertebrate synapses. To address this question, we performed extracellular focal recordings in cerebellar slices. The extracellular current consisted of a pre- (P1/N1) and postsynaptic (N2/SN) component. In
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Sheinin, Anton, Giuseppe Talani, Margaret I. Davis, and David M. Lovinger. "Endocannabinoid- and mGluR5-Dependent Short-Term Synaptic Depression in an Isolated Neuron/Bouton Preparation From the Hippocampal CA1 Region." Journal of Neurophysiology 100, no. 2 (2008): 1041–52. http://dx.doi.org/10.1152/jn.90226.2008.

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Endocannabinoids released from the postsynaptic neuronal membrane can activate presynaptic CB1 receptors and inhibit neurotransmitter release. In hippocampal slices, depolarization of the CA1 pyramidal neurons elicits an endocannabinoid-mediated inhibition of γ-aminobutyric acid release known as depolarization-induced suppression of inhibition (DSI). Using the highly reduced neuron/synaptic bouton preparation from the CA1 region of hippocampus, we have begun to examine endocannabinoid-dependent short-term depression (STD) of inhibitory synaptic transmission under well-controlled physiological
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Tang, Zheng-Quan, Hongxiang Gao, and Yong Lu. "Control of a Depolarizing GABAergic Input in an Auditory Coincidence Detection Circuit." Journal of Neurophysiology 102, no. 3 (2009): 1672–83. http://dx.doi.org/10.1152/jn.00419.2009.

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Neurons in the chicken nucleus laminaris (NL), the third-order auditory neurons that detect the interaural time differences that enable animals to localize sounds in the horizontal plane, receive glutamatergic excitation from the cochlear nucleus magnocellularis (NM) and GABAergic inhibition from the ipsilateral superior olivary nucleus. Here, we study metabotropic glutamate receptor (mGluR)- and GABAB receptor (GABABR)-mediated modulation of synaptic transmission in NL neurons. Gramicidin-perforated recordings from acute brain stem slice preparations showed that the reversal potential of the
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Hauser, Jessica L., Eleanore B. Edson, Bryan M. Hooks, and Chinfei Chen. "Metabotropic glutamate receptors and glutamate transporters shape transmission at the developing retinogeniculate synapse." Journal of Neurophysiology 109, no. 1 (2013): 113–23. http://dx.doi.org/10.1152/jn.00897.2012.

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Over the first few postnatal weeks, extensive remodeling occurs at the developing murine retinogeniculate synapse, the connection between retinal ganglion cells (RGCs) and the visual thalamus. Although numerous studies have described the role of activity in the refinement of this connection, little is known about the mechanisms that regulate glutamate concentration at and around the synapse over development. Here we show that interactions between glutamate transporters and metabotropic glutamate receptors (mGluRs) dynamically control the peak and time course of the excitatory postsynaptic curr
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Repicky, Sarah, and Kendal Broadie. "Metabotropic Glutamate Receptor–Mediated Use–Dependent Down-Regulation of Synaptic Excitability Involves the Fragile X Mental Retardation Protein." Journal of Neurophysiology 101, no. 2 (2009): 672–87. http://dx.doi.org/10.1152/jn.90953.2008.

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Loss of the mRNA-binding protein FMRP results in the most common inherited form of both mental retardation and autism spectrum disorders: fragile X syndrome (FXS). The leading FXS hypothesis proposes that metabotropic glutamate receptor (mGluR) signaling at the synapse controls FMRP function in the regulation of local protein translation to modulate synaptic transmission strength. In this study, we use the Drosophila FXS disease model to test the relationship between Drosophila FMRP (dFMRP) and the sole Drosophila mGluR (dmGluRA) in regulation of synaptic function, using two-electrode voltage-
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Dawei, Zhang, Hiroshi Kuromi, and Yoshiaki Kidokoro. "Presynaptic metabotropic glutamate receptors facilitate synaptic transmission at the Drosophila larval neuromuscular synapse." Neuroscience Research 31 (January 1998): S104. http://dx.doi.org/10.1016/s0168-0102(98)81942-1.

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Jonas, Peter. "The Time Course of Signaling at Central Glutamatergic Synapses." Physiology 15, no. 2 (2000): 83–89. http://dx.doi.org/10.1152/physiologyonline.2000.15.2.83.

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Glutamate is the main excitatory transmitter in the mammalian CNS, mediating fast synaptic transmission primarily by activation of AMPA-type glutamate receptor channels. Both synaptic structure and a cell-specific molecular switch in the AMPA receptor subunit expression are involved in the regulation of the synaptic signaling time course.
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Keable, Ryan, Iryna Leshchyns’ka, and Vladimir Sytnyk. "Trafficking and Activity of Glutamate and GABA Receptors: Regulation by Cell Adhesion Molecules." Neuroscientist 26, no. 5-6 (2020): 415–37. http://dx.doi.org/10.1177/1073858420921117.

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The efficient targeting of ionotropic receptors to postsynaptic sites is essential for the function of chemical excitatory and inhibitory synapses, constituting the majority of synapses in the brain. A growing body of evidence indicates that cell adhesion molecules (CAMs), which accumulate at synapses at the earliest stages of synaptogenesis, are critical for this process. A diverse variety of CAMs assemble into complexes with glutamate and GABA receptors and regulate the targeting of these receptors to the cell surface and synapses. Presynaptically localized CAMs provide an additional level o
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Neugebauer, Volker, Fatiha Zinebi, Rex Russell, Joel P. Gallagher, and Patricia Shinnick-Gallagher. "Cocaine and Kindling Alter the Sensitivity of Group II and III Metabotropic Glutamate Receptors in the Central Amygdala." Journal of Neurophysiology 84, no. 2 (2000): 759–70. http://dx.doi.org/10.1152/jn.2000.84.2.759.

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G-protein-coupled metabotropic glutamate receptors (mGluRs) are being implicated in various forms of neuroplasticity and CNS disorders. This study examined whether the sensitivities of mGluR agonists are modulated in a distinct fashion in different models of synaptic plasticity, specifically, kindling and chronic cocaine treatment. The influence of kindling and chronic cocaine exposure in vivo was examined in vitro on the modulation of synaptic transmission by group II and III metabotropic glutamate receptors using whole cell voltage-clamp recordings of central amygdala (CeA) neurons. Synaptic
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Raghavachari, Sridhar, and John E. Lisman. "Properties of Quantal Transmission at CA1 Synapses." Journal of Neurophysiology 92, no. 4 (2004): 2456–67. http://dx.doi.org/10.1152/jn.00258.2004.

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We have used Monte Carlo simulations to understand the generation of quantal responses at the single active zones of CA1 synapses. We constructed a model of AMPA channel activation that accounts for the responses to controlled glutamate application and a model of glutamate diffusion in the synaptic cleft. With no further adjustments to these models, we simulated the response to the release of glutamate from a single vesicle. The predicted response closely matches the rise time of observed responses, which recent measurements show is much faster (<100 μs) than previously thought. The simulat
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Kullmann, Dimitri M., Ming-Yuan Min, Fredrik Asztely, and Dmitri A. Rusakov. "Extracellular glutamate diffusion determines the occupancy of glutamate receptors at CA1 synapses in the hippocampus." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 354, no. 1381 (1999): 395–402. http://dx.doi.org/10.1098/rstb.1999.0392.

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Following exocytosis at excitatory synapses in the brain, glutamate binds to several subtypes of postsynaptic receptors. The degree of occupancy of AMPA and NMDA receptors at hippocampal synapses is, however, not known. One approach to estimate receptor occupancy is to examine quantal amplitude fluctuations of postsynaptic signals in hippocampal neurons studied in vitro . The results of such experiments suggest that NMDA receptors at CA1 synapses are activated not only by glutamate released from the immediately apposed presynaptic terminals, but also by glutamate spillover from neighbouring te
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Groc, Laurent, and Daniel Choquet. "Linking glutamate receptor movements and synapse function." Science 368, no. 6496 (2020): eaay4631. http://dx.doi.org/10.1126/science.aay4631.

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Regulation of neurotransmitter receptor content at synapses is achieved through a dynamic equilibrium between biogenesis and degradation pathways, receptor stabilization at synaptic sites, and receptor trafficking in and out synapses. In the past 20 years, the movements of receptors to and from synapses have emerged as a series of highly regulated processes that mediate postsynaptic plasticity. Our understanding of the properties and roles of receptor movements has benefited from technological advances in receptor labeling and tracking capacities, as well as from new methods to interfere with
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Reichelt, W., and T. Knöpfel. "Glutamate Uptake Controls Expression of a Slow Postsynaptic Current Mediated by mGluRs in Cerebellar Purkinje Cells." Journal of Neurophysiology 87, no. 4 (2002): 1974–80. http://dx.doi.org/10.1152/jn.00704.2001.

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At the cerebellar parallel fiber-Purkinje cell synapse, isolated presynaptic activity induces fast excitatory postsynaptic currents via ionotropic glutamate receptors while repetitive, high-frequency, presynaptic activity can also induce a slow excitatory postsynaptic current that is mediated by metabotropic glutamate receptors (mGluR1-EPSC). Here we investigated the involvement of glutamate uptake in the expression of the mGluR1-EPSC. Inhibitors of glutamate uptake led to a large increase of the mGluR1-EPSC. d-aspartate (0.4 mM) andl(−)-threo-3-hydroxyaspartate (0.4 mM) increased the mGluR1-E
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