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https://www.readbyqxmd.com/read/28063882/mice-lacking-grip1-2-show-increased-social-interactions-and-enhanced-phosphorylation-at-glua2-s880
#1
Mei Han, Rebeca Mejias, Shu-Ling Chiu, Rebecca Rose, Abby Adamczyk, Richard Huganir, Tao Wang
Glutamate receptor interacting proteins 1 and 2 (GRIP1/2) play an important role in regulating synaptic trafficking of AMPA receptor 2/3 (GluA2/3) and synaptic strength. Gain-of-function GRIP1 mutations are implicated in social behavioral deficits in autism. To study mechanisms of Grip1/2-mediated AMPA signaling in the regulation of social behaviors, we performed social behavioral testing on neuron-specific Grip1/2-double knockout (DKO) and wild type (WT) mice that are matched for age, sex, and strain background...
January 4, 2017: Behavioural Brain Research
https://www.readbyqxmd.com/read/28030475/spinal-intracellular-metabotropic-glutamate-receptor-5-mglur5-contributes-to-pain-and-c-fos-expression-in-a-rat-model-of-inflammatory-pain
#2
Kathleen Vincent, Shu Fan Wang, André Laferrière, Naresh Kumar, Terence J Coderre
Metabotropic glutamate receptor 5 (mGluR5) is an excitatory G-protein coupled receptor present in the spinal cord dorsal horn (SCDH) where it has a well-established role in pain. In addition to its traditional location on the cytoplasmic membrane, recent evidence shows that these receptors are present intracellularly on the nuclear membrane in the SCDH and are implicated in neuropathic pain. Nuclear mGluR5 is a functional receptor that binds glutamate entering the cell through the neuronal glutamate transporter (GT) EAAT3 and activates transcription factor c-fos, whereas plasma membrane mGluR5 is responsible for c-jun activation...
December 26, 2016: Pain
https://www.readbyqxmd.com/read/28028604/molecular-mechanisms-of-group-i-metabotropic-glutamate-receptor-mediated-ltp-and-ltd-in-basolateral-amygdala-in-vitro
#3
A Chen, W W Hu, X L Jiang, M Potegal, H Li
The roles of group I metabotropic glutamate receptors, metabotropic glutamate receptor 1 (mGluR1) and mGluR5, in regulating synaptic plasticity and metaplasticity in the basolateral amygdala (BLA) remain unclear. The present study examined mGluR1- and mGluR5-mediated synaptic plasticity in the BLA and their respective signaling mechanisms. Bath application of the group I mGluR agonist, 3,5-dihydroxyphenylglycine (DHPG) (20 μM), directly suppressed basal fEPSPs (84.5 ± 6.3% of the baseline). The suppressive effect persisted for at least 30 min after washout; it was abolished by the mGluR1 antagonist 7-(hydroxyimino)cyclopropa[b]chromen-1a-carboxylate ethyl ester (CPCCOEt) but was unaffected by the mGluR5 antagonist 2-methyl-6- (phenylethynyl)-pyridine (MPEP)...
December 28, 2016: Psychopharmacology
https://www.readbyqxmd.com/read/28011638/a-critical-role-for-ubiquitination-in-the-endocytosis-of-glutamate-receptors
#4
Ravinder Gulia, Rohan Sharma, Samarjit Bhattacharyya
Group I metabotropic glutamate receptors (mGluRs) play important roles in various neuronal processes and they elicit changes in synaptic efficacy through AMPAR endocytosis. Trafficking of mGluRs plays important roles in controlling the precise localization of these receptors at specific region of the cell as well as it regulates the activity of these receptors. Despite this obvious significance we know very little about the cellular mechanisms that control the trafficking of group I mGluRs. We show here that ligand-mediated internalization of group I mGluRs is ubiquitination dependent...
December 23, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28009293/calcium-release-from-stores-inhibits-girk
#5
Paul F Kramer, John T Williams
Synaptic transmission is mediated by ionotropic and metabotropic receptors that together regulate the rate and pattern of action potential firing. Metabotropic receptors can activate ion channels and modulate other receptors and channels. The present paper examines the interaction between group 1 mGluR-mediated calcium release from stores and GABAB/D2-mediated GIRK currents in rat dopamine neurons of the Substantia Nigra. Transient activation of mGluRs decreased the GIRK current evoked by GABAB and D2 receptors, although less efficaciously for D2...
December 20, 2016: Cell Reports
https://www.readbyqxmd.com/read/28008418/regulation-of-group-i-metabotropic-glutamate-receptors-by-mapk-erk-in-neurons
#6
Li-Min Mao, John Q Wang
Group I metabotropic glutamate receptors (mGluR1 and mGluR5 subtypes) are regulated by protein kinases. A recent focus is mitogen-activated protein kinases (MAPK). A prototypic subclass of MAPKs, extracellular signal-regulated kinases (ERK), is densely expressed in adult brain postmitotic neurons. This kinase resides in not only the cytoplasm around the nucleus, also the neuronal peripheral structures such as synapses. Recombinant ERK2 binds to C terminal tails of mGluR1a in vitro and native ERK1/2 forms complexes with mGluR1/5 in neurons in vivo...
2016: Journal of Nature and Science
https://www.readbyqxmd.com/read/28002633/vta-da-neuron-excitatory-synapses-in-shank3-%C3%AE-ex-4-9-mouse-line
#7
Bariselli Sebastiano, Bellone Camilla
SHANK3 proteins belong to the Shank/ProSAP family, which contain five-conserved domains - the ankyrin (ANK) repeated, the Src homology 3 (SH3), the PSD-95/Discs large/ZO-1 (PDZ), the proline-rich and the sterile alpha motif (SAM; Sheng and Kim, 2000). SHANK proteins are located at the postsynaptic density of excitatory synapses and indirectly link the metabotropic (mGluRs) and the ionotropic glutamate receptor (iGluRs: AMPARs, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, and NMDARs, N-methyl-D-aspartate receptors) via different domains (Naisbitt et al...
December 21, 2016: Synapse
https://www.readbyqxmd.com/read/27957526/mammalian-fmrp-s499-is-phosphorylated-by-ck2-and-promotes-secondary-phosphorylation-of-fmrp
#8
Christopher M Bartley, Rachel A O'Keefe, Anna Blice-Baum, Mihaela-Rita Mihailescu, Xuan Gong, Laura Miyares, Esra Karaca, Angélique Bordey
The fragile X mental retardation protein (FMRP) is an mRNA-binding regulator of protein translation that associates with 4-6% of brain transcripts and is central to neurodevelopment. Autism risk genes' transcripts are overrepresented among FMRP-binding mRNAs, and FMRP loss-of-function mutations are responsible for fragile X syndrome, the most common cause of monogenetic autism. It is thought that FMRP-dependent translational repression is governed by the phosphorylation of serine residue 499 (S499). However, recent evidence suggests that S499 phosphorylation is not modulated by metabotropic glutamate receptor class I (mGluR-I) or protein phosphatase 2A (PP2A), two molecules shown to regulate FMRP translational repression...
November 2016: ENeuro
https://www.readbyqxmd.com/read/27940363/evidence-for-presynaptically-silent-synapses-in-the-immature-hippocampus
#9
Jae Young Yoon, Sukwoo Choi
Silent synapses show NMDA receptor (NMDAR)-mediated synaptic responses, but not AMPAR-mediated synaptic responses. A prevailing hypothesis states that silent synapses contain NMDARs, but not AMPARs. However, alternative presynaptic hypotheses, according to which AMPARs are present at silent synapses, have been proposed; silent synapses show slow glutamate release via a fusion pore, and glutamate spillover from the neighboring synaptic terminals. Consistent with these presynaptic hypotheses, the peak glutamate concentrations at silent synapses have been estimated to be ≪170 μM, much lower than those seen at functional synapses...
January 22, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27936499/the-anatomy-of-mammalian-sweet-taste-receptors
#10
Jean-Baptiste Chéron, Jérôme Golebiowski, Serge Antonczak, Sébastien Fiorucci
All sweet-tasting compounds are detected by a single G-protein coupled receptor (GPCR), the heterodimer T1R2-T1R3, for which no experimental structure is available. The sweet taste receptor is a class C GPCR, and the recently published crystallographic structures of metabotropic glutamate receptor (mGluR) 1 and 5 provide a significant step forward for understanding structure-function relationships within this family. In this article, we recapitulate more than six hundred single point site-directed mutations and available structural data to obtain a critical alignment of the sweet taste receptor sequences with respect to other class C GPCRs...
December 9, 2016: Proteins
https://www.readbyqxmd.com/read/27886171/transduction-of-group-i-mglur-mediated-synaptic-plasticity-by-%C3%AE-arrestin2-signalling
#11
Andrew G Eng, Daniel A Kelver, Tristan P Hedrick, Geoffrey T Swanson
Conventional signalling by the group I metabotropic glutamate receptors, mGluR1 and mGluR5, occurs through G-protein coupling, but evidence suggests they might also utilize other, non-canonical effector pathways. Here we test whether group I mGluRs require β-arrestin signalling during specific forms of plasticity at hippocampal excitatory synapses. We find that genetic ablation of β-arrestin2, but not β-arrestin1, results in deficits in plasticity mediated by mGlu1 receptors in CA3 pyramidal neurons and by mGlu5 receptors in CA1 pyramidal neurons...
November 25, 2016: Nature Communications
https://www.readbyqxmd.com/read/27880915/blunted-mglur-activation-disinhibits-striatopallidal-transmission-in-parkinsonian-mice
#12
Qiaoling Cui, Jason E Pitt, Arin Pamukcu, Jean-Francois Poulin, Omar S Mabrouk, Michael P Fiske, Isabel B Fan, Elizabeth C Augustine, Katherine A Young, Robert T Kennedy, Rajeshwar Awatramani, C Savio Chan
The prevailing circuit model predicts that hyperactivity of the striatopallidal pathway and subsequently increased inhibition of external globus pallidus (GPe) neurons lead to the hypokinetic symptoms of Parkinson's disease (PD). It is believed that hyperactivity of the striatopallidal pathway is due to inactivity of dopamine receptors on the somatodendritic membrane of striatopallidal neurons, but the exact cellular underpinnings remain unclear. In this study, we show that mouse GPe astrocytes critically control ambient glutamate level, which in turn gates striatopallidal transmission via the activation of presynaptic metabotropic glutamate receptors...
November 22, 2016: Cell Reports
https://www.readbyqxmd.com/read/27872582/separate-ionotropic-and-metabotropic-glutamate-receptor-functions-in-depotentiation-vs-ltp-a-distinct-role-for-group1-mglur-subtypes-and-nmdars
#13
Amira Latif-Hernandez, Enrico Faldini, Tariq Ahmed, Detlef Balschun
Depotentiation (DP) is a mechanism by which synapses that have recently undergone long-term potentiation (LTP) can reverse their synaptic strengthening within a short time-window after LTP induction. Group 1 metabotropic glutamate receptors (mGluRs) were shown to be involved in different forms of LTP and long-term depression (LTD), but little is known about their roles in DP. Here, we generated DP by applying low-frequency stimulation (LFS) at 5 Hz after LTP had been induced by a single train of theta-burst-stimulation (TBS)...
2016: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/27872019/metabotropic-glutamate-receptors-and-neurodegenerative-diseases
#14
REVIEW
Fabiola M Ribeiro, Luciene B Vieira, Rita G W Pires, Roenick P Olmo, Stephen S G Ferguson
Glutamate is the most important excitatory neurotransmitter of the mammalian central nervous system (CNS), playing an important role in memory, synaptic plasticity and neuronal development. However, glutamate overstimulation is also implicated in neuronal cell death. There are two major types of glutamate receptors: ionotropic and metabotropic. Thus far, eight metabotropic glutamate receptors (mGluRs) subtypes have been characterized and are divided into three subgroups based on sequence homology and cell signaling activation...
January 2017: Pharmacological Research: the Official Journal of the Italian Pharmacological Society
https://www.readbyqxmd.com/read/27866902/the-atypical-antipsychotic-olanzapine-disturbs-depotentiation-by-modulating-machrs-and-impairs-reversal-learning
#15
Woo Seok Song, Jin Hee Cha, Sang Ho Yoon, Young Seon Cho, Kyeong-Yeol Park, Myoung-Hwan Kim
Antipsychotic medication is an essential component for treating schizophrenia, which is a serious mental disorder that affects approximately 1% of the global population. Olanzapine (Olz), one of the most frequently prescribed atypical antipsychotics, is generally considered a first-line drug for treating schizophrenia. In contrast to psychotic symptoms, the effects of Olz on cognitive symptoms of schizophrenia are still unclear. In addition, the mechanisms by which Olz affects the neural circuits associated with cognitive function are unknown...
March 1, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/27856517/mglur-long-term-depression-regulates-glua2-association-with-copii-vesicles-and-exit-from-the-endoplasmic-reticulum
#16
Joseph E Pick, Latika Khatri, Matheus F Sathler, Edward B Ziff
mGluR long-term depression (mGluR-LTD) is a form of synaptic plasticity induced at excitatory synapses by metabotropic glutamate receptors (mGluRs). mGluR-LTD reduces synaptic strength and is relevant to learning and memory, autism, and sensitization to cocaine; however, the mechanism is not known. Here we show that activation of Group I mGluRs in medium spiny neurons induces trafficking of GluA2 from the endoplasmic reticulum (ER) to the synapse by enhancing GluA2 binding to essential COPII vesicle proteins, Sec23 and Sec13...
January 17, 2017: EMBO Journal
https://www.readbyqxmd.com/read/27847432/metabotropic-glutamate-receptor-dependent-long-term-depression-in-the-cortex
#17
REVIEW
Sukjae Joshua Kang, Bong-Kiun Kaang
Metabotropic glutamate receptor (mGluR)-dependent long-term depression (LTD), a type of synaptic plasticity, is characterized by a reduction in the synaptic response, mainly at the excitatory synapses of the neurons. The hippocampus and the cerebellum have been the most extensively studied regions in mGluR-dependent LTD, and Group 1 mGluR has been reported to be mainly involved in this synaptic LTD at excitatory synapses. However, mGluR-dependent LTD in other brain regions may be involved in the specific behaviors or diseases...
November 2016: Korean Journal of Physiology & Pharmacology
https://www.readbyqxmd.com/read/27807414/depotentiation-from-potentiated-synaptic-strength-in-a-tristable-system-of-coupled-phosphatase-and-kinase
#18
Mengjiao Chen, Wei Ren, Xingang Wang
Long-term potentiation (LTP) of synaptic strength is strongly implicated in learning and memory. On the other hand, depotentiation, the reversal of synaptic strength from potentiated LTP state to the pre-LTP level, is required in extinction of the obsolete memory. A generic tristable system, which couples the phosphatase and kinase switches, exclusively explains how moderate and high elevation of intracellular calcium concentration triggers long-term depression (LTD) and LTP, respectively. The present study, introducing calcium influx and calcium release from internal store into the tristable system, further show that significant elevation of cytoplasmic calcium concentration switches activation of both kinase and phosphatase to their basal states, thereby depotentiate the synaptic strength...
2016: Frontiers in Computational Neuroscience
https://www.readbyqxmd.com/read/27798131/cocaine-exposure-enhances-the-activity-of-ventral-tegmental-area-dopamine-neurons-via-calcium-impermeable-nmdars
#19
Meaghan Creed, Jennifer Kaufling, Giulia R Fois, Marion Jalabert, Tifei Yuan, Christian Lüscher, Francois Georges, Camilla Bellone
: Potentiation of excitatory inputs onto dopamine neurons of the ventral tegmental area (VTA) induced by cocaine exposure allows remodeling of the mesocorticolimbic circuitry, which ultimately drives drug-adaptive behavior. This potentiation is mediated by changes in NMDAR and AMPAR subunit composition. It remains unknown how this synaptic plasticity affects the activity of dopamine neurons. Here, using rodents, we demonstrate that a single cocaine injection increases the firing rate and bursting activity of VTA dopamine neurons, and that these increases persist for 7 d...
October 19, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/27781556/mood-therapeutics-novel-pharmacological-approaches-for-treating-depression
#20
Ioline D Henter, Rafael T de Sousa, Philip W Gold, Andre R Brunoni, Carlos A Zarate, Rodrigo Machado-Vieira
Real-world effectiveness trials suggest that antidepressant efficacy is limited in many patients with mood disorders, underscoring the urgent need for novel therapeutics to treat these disorders. Areas Covered: Here, we review the clinical evidence supporting the use of novel modulators for the treatment of mood disorders, including specific glutamate modulators such as: 1) high-trapping glutamatergic modulators; 2) subunit (NR2B)-specific N-methyl-D-aspartate (NMDA) receptor antagonists; 3) NMDA receptor glycine-site partial agonists; and 4) metabotropic glutamate receptor (mGluR) modulators...
October 26, 2016: Expert Review of Clinical Pharmacology
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