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Journal articles on the topic 'MGluR-mediated priming of LTP'

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1

Auerbach, Benjamin D., and Mark F. Bear. "Loss of the Fragile X Mental Retardation Protein Decouples Metabotropic Glutamate Receptor Dependent Priming of Long-Term Potentiation From Protein Synthesis." Journal of Neurophysiology 104, no. 2 (2010): 1047–51. http://dx.doi.org/10.1152/jn.00449.2010.

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Fragile X Syndrome (FXS), the most common inherited form of intellectual disability, is caused by loss of the fragile X mental retardation protein (FMRP). FMRP is a negative regulator of local mRNA translation downstream of group 1 metabotropic glutamate receptor (Gp1 mGluR) activation. In the absence of FMRP there is excessive mGluR-dependent protein synthesis, resulting in exaggerated mGluR-dependent long-term synaptic depression (LTD) in area CA1 of the hippocampus. Understanding disease pathophysiology is critical for development of therapies for FXS and the question arises of whether it i
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2

Cohen, A. S., and W. C. Abraham. "Facilitation of long-term potentiation by prior activation of metabotropic glutamate receptors." Journal of Neurophysiology 76, no. 2 (1996): 953–62. http://dx.doi.org/10.1152/jn.1996.76.2.953.

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1. The influence of prior metabotropic glutamate receptor (mGluR) activation on subsequent long-term potentiation (LTP) induction was investigated with the use of the mGluR agonist 1-amino-cyclopentane-1S,3R-dicarboxylic acid (ACPD, 20 microM). Field potential recordings were made in the stratum radiatum of CA1 slices taken from young adult male rats and from which CA3 was routinely dissected. Theta burst stimulation (TBS) just above threshold was used to induce LTP. 2. A 10-min bath application of ACPD begun 30 min before the TBS facilitated the induction of LTP in a dose-dependent manner and
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3

Cohen, Akiva S., Christine M. Coussens, Clarke R. Raymond, and Wickliffe C. Abraham. "Long-Lasting Increase in Cellular Excitability Associated With the Priming of LTP Induction in Rat Hippocampus." Journal of Neurophysiology 82, no. 6 (1999): 3139–48. http://dx.doi.org/10.1152/jn.1999.82.6.3139.

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The mechanisms underlying the facilitation (priming) of long-term potentiation (LTP) by prior activation of metabotropic glutamate receptors (mGluRs) were investigated in area CA1 of rat hippocampal slices. In particular, we focused on whether a long-lasting increase in postsynaptic excitability could account for the facilitated LTP. Administration of the mGluR agonist 1S,3R-aminocyclopentanedicarboxylic acid (ACPD) produced rapid decreases in the amplitude of both the slow spike afterhyperpolarization (AHPslow) and spike frequency adaptation recorded intracellularly from CA1 pyramidal cells.
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4

Hu, Bin, Sergei Karnup, Lei Zhou, and Armin Stelzer. "Reversal of Hippocampal LTP by Spontaneous Seizure-Like Activity: Role of Group I mGluR and Cell Depolarization." Journal of Neurophysiology 93, no. 1 (2005): 316–36. http://dx.doi.org/10.1152/jn.00172.2004.

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Memory impairment is a common consequence of epileptic seizures. The hippocampal formation is particularly prone to seizure-induced amnesia due to its prominent role in mnemonic processes. We used the isolated CA1 slice preparation to examine effects of seizure-like activity on hippocampal plasticity, long-term potentiation (LTP), and long-term depression (LTD). Repeated spontaneous ictal events, generated in the presence of antagonists of GABAA receptor function, led to a stepwise erasure of LTP (termed spontaneous depotentiation, SDP). SDP could be initiated at various stages of LTP consolid
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5

IV, Paul M. Lea, Barbara Wroblewska, John M. Sarvey та Joseph H. Neale. "β-NAAG Rescues LTP From Blockade by NAAG in Rat Dentate Gyrus via the Type 3 Metabotropic Glutamate Receptor". Journal of Neurophysiology 85, № 3 (2001): 1097–106. http://dx.doi.org/10.1152/jn.2001.85.3.1097.

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N-Acetylaspartylglutamate (NAAG) is an agonist at the type 3 metabotropic glutamate receptor (mGluR3), which is coupled to a Gi/o protein. When activated, the mGluR3 receptor inhibits adenylyl cyclase and reduces the cAMP-mediated second-messenger cascade. Long-term potentiation (LTP) in the medial perforant path (MPP) of the hippocampal dentate gyrus requires increases in cAMP. The presence of mGluR3 receptors and NAAG in neurons of the dentate gyrus suggests that this peptide transmitter may inhibit LTP in the dentate gyrus. High-frequency stimulation (100 Hz; 2 s) of the MPP resulted in LTP
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6

Neugebauer, Volker, N. Bradley Keele, and Patricia Shinnick-Gallagher. "Loss of Long-Lasting Potentiation Mediated by Group III mGluRs in Amygdala Neurons in Kindling-Induced Epileptogenesis." Journal of Neurophysiology 78, no. 6 (1997): 3475–78. http://dx.doi.org/10.1152/jn.1997.78.6.3475.

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Neugebauer, Volker, N. Bradley Keele, and Patricia Shinnick-Gallagher. Loss of long-lasting potentiation mediated by group III mGluRs in amygdala neurons in kindling-induced epileptogenesis. J. Neurophysiol. 78: 3475–3478, 1997. Long-lasting modifications of synaptic transmission can be induced in the amygdala by electrical stimulation as done in the long-term potentiation (LTP) model of learning and memory and the kindling model of epilepsy. The present study reports for the first time a long-lasting potentiation (LLP) of synaptic transmission that is induced pharmacologically by the activati
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7

Harrison, John M., Richard G. Allen, Michael J. Pellegrino, John T. Williams, and Olivier J. Manzoni. "Chronic Morphine Treatment Alters Endogenous Opioid Control of Hippocampal Mossy Fiber Synaptic Transmission." Journal of Neurophysiology 87, no. 5 (2002): 2464–70. http://dx.doi.org/10.1152/jn.2002.87.5.2464.

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Synaptic adaptations are thought to be an important component of the consequences of drug abuse. One such adaptation is an up-regulation of adenylyl cyclase that has been shown to increase transmitter release at several inhibitory synapses. In this study the effects of chronic morphine treatment were studied on mossy fiber synapses in the guinea pig hippocampus using extracellular field potential recordings. This opioid-sensitive synapse was chosen because of the known role of the adenylyl cyclase cascade in the regulation of glutamate release. Long-term potentiation (LTP) at the mossy fiber s
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8

Vickery, R. M., Shanida H. Morris, and Lynn J. Bindman. "Metabotropic Glutamate Receptors Are Involved in Long-Term Potentiation in Isolated Slices of Rat Medial Frontal Cortex." Journal of Neurophysiology 78, no. 6 (1997): 3039–46. http://dx.doi.org/10.1152/jn.1997.78.6.3039.

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Vickery, R. M., Shanida H. Morris, and Lynn J. Bindman. Metabotropic glutamate receptors are involved in long-term potentiation in isolated slices of rat medial frontal cortex. J. Neurophysiol. 78: 3039–3046, 1997. The prelimbic region of medial frontal cortex in the rat receives a direct input from the hippocampus and this functional connection is essential for aspects of spatial memory. Activity-dependent changes in the effectiveness of synaptic transmission in the medial frontal cortex, namely long-term potentiation (LTP) and long-term depression (LTD) can persist for tens of minutes or hou
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9

Chinestra, P., L. Aniksztejn, D. Diabira, and Y. Ben-Ari. "(RS)-alpha-methyl-4-carboxyphenylglycine neither prevents induction of LTP nor antagonizes metabotropic glutamate receptors in CA1 hippocampal neurons." Journal of Neurophysiology 70, no. 6 (1993): 2684–89. http://dx.doi.org/10.1152/jn.1993.70.6.2684.

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1. The effects of the putative antagonist of metabotropic glutamate receptors (mGluR), (RS)-alpha-methyl-4-carboxyphenylglycine (MCPG), were investigated in CA1 hippocampal neurons using intracellular and extracellular recordings. 2. MCPG (0.5 mM) did not antagonize the characteristic block of the slow afterhyperpolarization and spike accomodation produced by the selective mGluR agonist, 1S,3R-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) (30 microM). 3. MCPG (0.5 mM) did not prevent the inward current produced by 1S,3R-ACPD (30 microM) [240 +/- 14 and 255 +/- 21 pA (mean +/- SD) in t
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10

Cumiskey, Derval, Mark Pickering, and John J. O’Connor. "Interleukin-18 mediated inhibition of LTP in the rat dentate gyrus is attenuated in the presence of mGluR antagonists." Neuroscience Letters 412, no. 3 (2007): 206–10. http://dx.doi.org/10.1016/j.neulet.2006.11.007.

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11

Gumenscheimer, Marina, Ivan Mitov, Chris Galanos, and Marina A. Freudenberg. "Beneficial or Deleterious Effects of a Preexisting Hypersensitivity to Bacterial Components on the Course and Outcome of Infection." Infection and Immunity 70, no. 10 (2002): 5596–603. http://dx.doi.org/10.1128/iai.70.10.5596-5603.2002.

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ABSTRACT Priming with heat-killed Propionibacterium acnes enhances the sensitivity of mice to lipopolysaccharide (LPS) and other biologically active bacterial components. We show that P. acnes priming has protective and deleterious effects on a subsequent serovar Typhimurium infection. It may result in a complete protection or prolonged survival, or it may accelerate mortality of the infected mice, depending on the number of serovar Typhimurium bacteria administered and on the degree of LPS hypersensitivity at the time of infection. Both effects of P. acnes-induced hypersensitivity are mediate
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12

Jiang, Xiangzhi, Wei Lin, Yuanyuan Cheng, and Dongming Wang. "mGluR5 Facilitates Long-Term Synaptic Depression in a Stress-Induced Depressive Mouse Model." Canadian Journal of Psychiatry 65, no. 5 (2019): 347–55. http://dx.doi.org/10.1177/0706743719874162.

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Background Glutamatergic system has been known to play a role in the pathogenesis of major depression disorder by inducing N-methyl-d-aspartate receptor-dependent long-term depression (LTD) or metabotropic glutamate receptors (mGluR)-dependent LTD. Here, we characterized the LTD in a chronic social defeat stress (CSDS)-induced depressive mouse model. Methods CSDS was used to induce the depressive-like behaviors in C57BL/6 male mice, which were assessed using sucrose preference test and social interaction test. The synaptic strength including LTD and long-term potentiation (LTP) induced by pair
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13

de Haas, Carla J. C., Miriam J. J. G. Poppelier, Kok P. M. van Kessel, and Jos A. G. van Strijp. "Serum Amyloid P Component Prevents High-Density Lipoprotein-Mediated Neutralization of Lipopolysaccharide." Infection and Immunity 68, no. 9 (2000): 4954–60. http://dx.doi.org/10.1128/iai.68.9.4954-4960.2000.

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ABSTRACT Lipopolysaccharide (LPS) is an amphipathic macromolecule that is highly aggregated in aqueous preparations. LPS-binding protein (LBP) catalyzes the transfer of single LPS molecules, segregated from an LPS aggregate, to high-density lipoproteins (HDL), which results in the neutralization of LPS. When fluorescein isothiocyanate-labeled LPS (FITC-LPS) is used, this transfer of LPS monomers to HDL can be measured as an increase in fluorescence due to dequenching of FITC-LPS. Recently, serum amyloid P component (SAP) was shown to neutralize LPS in vitro, although only in the presence of lo
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14

Karshovska, Ela, Jaroslav Pelisek, Miriam Koch, et al. "CCR6 selectively promotes monocyte mediated inflammation and atherogenesis in mice." Thrombosis and Haemostasis 110, no. 12 (2013): 1267–77. http://dx.doi.org/10.1160/th13-01-0017.

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SummaryThe chemokine receptor CCR6 is expressed by various cell subsets implicated in atherogenesis, such as monocytes, Th17 and regulatory T cells. In order to further define the role of CCR6 in atherosclerosis, CCR6-deficient (Ccr6 -/-) mice were crossed with low-density lipoprotein receptor-deficient (Ldlr -/-) mice to generate atherosclerosis-prone mice deficient in CCR6. Compared to Ldlr -/- controls, atherosclerotic burden in the aortic sinus and aorta were reduced in Ccr6 -/- Ldlr -/- mice fed a high fat diet, associated with a profound depression in lesional macrophage accumulation. Lo
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15

Emily, Mavin, Lindsay Nicholson, Rafez Ahmed, Matthew Collin, Anne Dickinson, and Xiao-nong Wang. "Treg Induced Impairment of DC Function and Its Impact on GvH Reactions." Blood 124, no. 21 (2014): 3815. http://dx.doi.org/10.1182/blood.v124.21.3815.3815.

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Abstract Promising results from murine models and early stage clinical trials have shown that adoptive transfer of regulatory T cells (Treg) prevents graft-versus-host disease (GvHD). However, the primary target of Treg mediated protection against GvHD is yet to be fully defined. We have previously shown that the presence of Treg during effector T cell priming is able to ameliorate cutaneous GvH reactions in vitro by blocking effector cell migration. This has led to the hypothesis that Treg modulation of dendritic cells (DC) could be a key mechanism by which Treg exert their protective role in
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16

Ishii, Chiaki, Natsumi Shibano, Mio Yamazaki, et al. "CAPS1 is involved in hippocampal synaptic plasticity and hippocampus-associated learning." Scientific Reports 11, no. 1 (2021). http://dx.doi.org/10.1038/s41598-021-88009-w.

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AbstractCalcium-dependent activator protein for secretion 1 (CAPS1) is a key molecule in vesicular exocytosis, probably in the priming step. However, CAPS1’s role in synaptic plasticity and brain function is elusive. Herein, we showed that synaptic plasticity and learning behavior were impaired in forebrain and/or hippocampus-specific Caps1 conditional knockout (cKO) mice by means of molecular, physiological, and behavioral analyses. Neonatal Caps1 cKO mice showed a decrease in the number of docked vesicles in the hippocampal CA3 region, with no detectable changes in the distribution of other
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17

Ranieri, Federico, Sara Mariotto, Raffaele Dubbioso, and Vincenzo Di Lazzaro. "Brain Stimulation as a Therapeutic Tool in Amyotrophic Lateral Sclerosis: Current Status and Interaction With Mechanisms of Altered Cortical Excitability." Frontiers in Neurology 11 (February 5, 2021). http://dx.doi.org/10.3389/fneur.2020.605335.

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In the last 20 years, several modalities of neuromodulation, mainly based on non-invasive brain stimulation (NIBS) techniques, have been tested as a non-pharmacological therapeutic approach to slow disease progression in amyotrophic lateral sclerosis (ALS). In both sporadic and familial ALS cases, neurophysiological studies point to motor cortical hyperexcitability as a possible priming factor in neurodegeneration, likely related to dysfunction of both excitatory and inhibitory mechanisms. A trans-synaptic anterograde mechanism of excitotoxicity is thus postulated, causing upper and lower moto
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18

Dasgupta, Ananya, Yu Jia Lim, Krishna Kumar, et al. "Group III metabotropic glutamate receptors gate long-term potentiation and synaptic tagging/capture in rat hippocampal area CA2." eLife 9 (April 20, 2020). http://dx.doi.org/10.7554/elife.55344.

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Metabotropic glutamate receptors (mGluRs) play an important role in synaptic plasticity and memory and are largely classified based on amino acid sequence homology and pharmacological properties. Among group III metabotropic glutamate receptors, mGluR7 and mGluR4 show high relative expression in the rat hippocampal area CA2. Group III metabotropic glutamate receptors are known to down-regulate cAMP-dependent signaling pathways via the activation of Gi/o proteins. Here, we provide evidence that inhibition of group III mGluRs by specific antagonists permits an NMDA receptor- and protein synthesi
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