Relevant bibliographies by topics / MGlu2 receptor

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Academic literature on the topic 'MGlu2 receptor'

Author: Grafiati
Published: 1 February 2023

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Journal articles on the topic "MGlu2 receptor"

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Bruno, Valeria, Giuseppe Battaglia, Agata Copani, Mara D'Onofrio, P. Di Iorio, Antonio De Blasi, Daniela Melchiorri, Peter J. Flor, and Ferdinando Nicoletti. "Metabotropic Glutamate Receptor Subtypes as Targets for Neuroprotective Drugs." Journal of Cerebral Blood Flow & Metabolism 21, no. 9 (September 2001): 1013–33. http://dx.doi.org/10.1097/00004647-200109000-00001.

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Metabotropic glutamate (mGlu) receptors have been considered as potential targets for neuroprotective drugs, but the lack of specific drugs has limited the development of neuroprotective strategies in experimental models of acute or chronic central nervous system (CNS) disorders. The advent of potent and centrally available subtype-selective ligands has overcome this limitation, leading to an extensive investigation of the role of mGlu receptor subtypes in neurodegeneration during the last 2 years. Examples of these drugs are the noncompetitive mGlu1 receptor antagonists, CPCCOEt and BAY-36-7620; the noncompetitive mGlu5 receptor antagonists, 2-methyl-6-(phenylethynyl)pyridine, SIB-1893, and SIB-1757; and the potent mGlu2/3 receptor agonists, LY354740 and LY379268. Pharmacologic blockade of mGlu1 or mGlu5 receptors or pharmacologic activation of mGlu2/3 or mGlu4/7/8 receptors produces neuroprotection in a variety of in vitro or in vivo models. MGlu1 receptor antagonists are promising drugs for the treatment of brain ischemia or for the prophylaxis of neuronal damage induced by synaptic hyperactivity. MGlu5 receptor antagonists may limit neuronal damage induced by a hyperactivity of N-methyl-d-aspartate (NMDA) receptors, because mGlu5 and NMDA receptors are physically and functionally connected in neuronal membranes. A series of observations suggest a potential application of mGlu5 receptor antagonists in chronic neurodegenerative disorders, such as amyotrophic lateral sclerosis and Alzheimer disease. MGlu2/3 receptor agonists inhibit glutamate release, but also promote the synthesis and release of neurotrophic factors in astrocytes. These drugs may therefore have a broad application as neuroprotective agents in a variety of CNS disorders. Finally, mGlu4/7/8 receptor agonists potently inhibit glutamate release and have a potential application in seizure disorders. The advantage of all these drugs with respect to NMDA or AMPA receptor agonists derives from the evidence that mGlu receptors do not “mediate,” but rather “modulate” excitatory synaptic transmission. Therefore, it can be expected that mGlu receptor ligands are devoid of the undesirable effects resulting from the inhibition of excitatory synaptic transmission, such as sedation or an impairment of learning and memory.
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Chaki, Shigeyuki, Hiroyuki Koike, and Kenichi Fukumoto. "Targeting of Metabotropic Glutamate Receptors for the Development of Novel Antidepressants." Chronic Stress 3 (January 2019): 247054701983771. http://dx.doi.org/10.1177/2470547019837712.

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Since discovering that ketamine has robust antidepressant effects, the glutamatergic system has been proposed as an attractive target for the development of novel antidepressants. Among the glutamatergic system, metabotropic glutamate (mGlu) receptors are of interest because mGlu receptors play modulatory roles in glutamatergic transmission, consequently, agents acting on mGlu receptors might not exert the adverse effects associated with ketamine. mGlu receptors have eight subtypes that are classified into three groups, and the roles of each mGlu receptor subtype in depression are being investigated. To date, the potential use of mGlu5 receptor antagonists and mGlu2/3 receptor antagonists as antidepressants has been actively investigated, and the mechanisms underlying these antidepressant effects are being delineated. Although the outcomes of clinical trials using an mGlu5 receptor negative allosteric modulator and an mGlu2/3 receptor negative allosteric modulator have not been encouraging, these trials have been inconclusive, and additional trials using other compounds with more appropriate profiles are needed. In contrast, the roles of group III mGlu receptors have not yet been fully elucidated because of a lack of suitable pharmacological tools. Nonetheless, investigations of the use of mGlu4 and mGlu7 receptors as drug targets for the development of antidepressants have been ongoing, and some interesting evidence has been obtained.
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Hagena, Hardy, and Denise Manahan-Vaughan. "Role of mGlu5 in Persistent Forms of Hippocampal Synaptic Plasticity and the Encoding of Spatial Experience." Cells 11, no. 21 (October 24, 2022): 3352. http://dx.doi.org/10.3390/cells11213352.

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The metabotropic glutamate (mGlu) receptor family consists of group I receptors (mGlu1 and mGlu5) that are positively coupled to phospholipase-C and group II (mGlu2 and mGlu3) and III receptors (mGlu4-8) that are negatively coupled to adenylyl cyclase. Of these, mGlu5 has emerged as a key factor in the induction and maintenance of persistent (> 24 h) forms of hippocampal synaptic plasticity. Studies in freely behaving rodents have revealed that mGlu5 plays a pivotal role in the stabilisation of hippocampal long-term potentiation (LTP) and long-term depression (LTD) that are tightly associated with the acquisition and retention of knowledge about spatial experience. In this review article we shall address the state of the art in terms of the role of mGlu5 in forms of hippocampal synaptic plasticity related to experience-dependent information storage and present evidence that normal mGlu5 function is central to these processes.
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Johnson, M. P., E. S. Nisenbaum, T. H. Large, R. Emkey, M. Baez, and A. E. Kingston. "Allosteric modulators of metabotropic glutamate receptors: lessons learnt from mGlu1, mGlu2 and mGlu5 potentiators and antagonists." Biochemical Society Transactions 32, no. 5 (October 26, 2004): 881–87. http://dx.doi.org/10.1042/bst0320881.

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Although relatively few G-protein-coupled receptors are Class C, in recent years, this small family of receptors has become a focal point for the discovery of new and exciting allosteric modulators. The mGlu (metabotropic glutamate) receptors are illustrative in the discovery of both positive and/or negative allosteric modulators with unique pharmacological properties. For instance, allosteric modulators of the mGlu2 receptor act as potentiators of glutamate responses in clonal expression systems and in native tissue assays. These potentiators act to increase the affinity of orthosteric agonists for the mGlu2 receptor and shift potency curves for the agonist to the left. In electrophysiological experiments, the potentiators show a unique activation-state-dependent presynaptic inhibition of glutamate release and significantly enhance the receptor-mediated increase in G-protein binding, as seen with autoradiography. Similarly, potentiators of mGlu5 have been described, as well as allosteric antagonists or inverse agonists of mGlu1 and mGlu5. Binding and activity of the modulators have recently indicated that positive and negative allosteric sites can be, but are not necessarily, overlapping. Compared with orthosteric ligands, these modulators display a unique degree of subtype selectivity within the highly conserved mGlu family of receptors and can have very distinct pharmacological properties, such as neuronal frequency-dependent activity. This short review describes some of the unique features of these mGlu1, mGlu2 and mGlu5 allosteric modulators.
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Xiang, Zixiu, Xiaohui Lv, Xin Lin, Daniel E. O’Brien, Molly K. Altman, Craig W. Lindsley, Jonathan A. Javitch, Colleen M. Niswender, and P. Jeffrey Conn. "Input-specific regulation of glutamatergic synaptic transmission in the medial prefrontal cortex by mGlu2/mGlu4 receptor heterodimers." Science Signaling 14, no. 677 (April 6, 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 within the rodent medial prefrontal cortex (mPFC). Activation of mGlu2/mGlu4 heterodimers inhibited glutamatergic signaling at thalamo-mPFC synapses but not at hippocampus-mPFC or amygdala-mPFC synapses. These findings raise the possibility that selectively targeting these heterodimers could be a therapeutic strategy for some neurologic and neuropsychiatric disorders involving specific brain circuits.
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Storto, M., M. Sallese, L. Salvatore, R. Poulet, DF Condorelli, P. Dell'Albani, MF Marcello, et al. "Expression of metabotropic glutamate receptors in the rat and human testis." Journal of Endocrinology 170, no. 1 (July 1, 2001): 71–78. http://dx.doi.org/10.1677/joe.0.1700071.

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The G protein-coupled receptor kinase type 4 mediates the homologous desensitisation of type-1 metabotropic glutamate (mGlu1) receptors and is predominantly expressed in the testis. Hence, we searched for the expression of mGlu1 or other mGlu receptor subtypes in rat and human testes. RT-PCR analysis showed the presence of mGlu1, -4 and -5 (but not -2 or -3) receptor mRNA in the rat testis. The presence of mGlu1 and -5 (but not mGlu2/3) receptor proteins was also demonstrated by Western blot analysis. In the rat testis, both mGlu1a and -5 receptors were highly expressed in cells of the germinal line. It is likely that these receptors are functional, because the agonist, (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid, was able to stimulate inositol phospholipid hydrolysis in slices prepared from rat testes. Immunocytochemical analysis of bioptic samples from human testes showed a high expression of mGlu5 receptors inside the seminiferous tubuli, whereas mGlu1a immunoreactivity was restricted to intertubular spaces. mGlu5 receptors were also present in mature spermatozoa, where they were localised in the mid-piece and tail. This localisation coincided with that of beta-arrestin, a protein that is critically involved in the homologous desensitisation and internalisation of G protein-coupled receptors. Taken collectively, these results offer the first evidence for the expression of any glutamate receptor in testes, and suggest that at least mGlu5 receptors are present and functionally active in mature human sperm.
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Marciniak, Marcin, Barbara Chruścicka, Tomasz Lech, Grzegorz Burnat, and Andrzej Pilc. "Expression of group III metabotropic glutamate receptors in the reproductive system of male mice." Reproduction, Fertility and Development 28, no. 3 (2016): 369. http://dx.doi.org/10.1071/rd14132.

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Although the presence of metabotropic glutamate (mGlu) receptors in the central nervous system is well documented, they have recently been found in peripheral and non-neuronal tissues. In the present study we investigated the expression of group III mGlu receptors in the reproductive system of male mice. Reverse transcription–polymerase chain reaction analysis revealed the presence of mGlu6, mGlu7 and mGlu8 (but not mGlu4) receptor transcripts in testes and epididymides from adult mice. In addition, expression of mGlu6 (Grm6) and mGlu8 receptor (Grm8) mRNA was detected in spermatozoa isolated from the vas deferens. The vas deferens was found to contain only mGlu7 receptor (Grm7) mRNA, which was particularly intense in 21-day-old male mice. In penile homogenates, only the mGlu7 receptor signal was detected. Genetic ablation of the mGlu7 receptor in males led to fertility disorders manifested by decreased insemination capability as well as deterioration of sperm parameters, particularly sperm motility, vitality, sperm membrane integrity and morphology, with a simultaneous increase in sperm concentration. These results indicate that constitutively expressed mGlu receptors in the male reproductive system may play an important role in ejaculation and/or erection processes, as well as in the formation and maturation of spermatozoa.
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Hofmann, Christopher S., Sheridan Carrington, Andrew N. Keller, Karen J. Gregory, and Colleen M. Niswender. "Regulation and functional consequences of mGlu4 RNA editing." RNA 27, no. 10 (July 8, 2021): 1220–40. http://dx.doi.org/10.1261/rna.078729.121.

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Metabotropic glutamate receptor 4 (mGlu4) is one of eight mGlu receptors within the Class C G protein-coupled receptor superfamily. mGlu4 is primarily localized to the presynaptic membrane of neurons where it functions as an auto and heteroreceptor controlling synaptic release of neurotransmitter. mGlu4 is implicated in numerous disorders and is a promising drug target; however, more remains to be understood about its regulation and pharmacology. Using high-throughput sequencing, we have validated and quantified an adenosine-to-inosine (A-to-I) RNA editing event that converts glutamine 124 to arginine in mGlu4; additionally, we have identified a rare but novel K129R site. Using an in vitro editing assay, we then validated the pre-mRNA duplex that allows for editing by ADAR enzymes and predicted its conservation across the mammalian species. Structural modeling of the mGlu4 protein predicts the Q124R substitution to occur in the B helix of the receptor that is critical for receptor dimerization and activation. Interestingly, editing of a receptor homodimer does not disrupt G protein activation in response to the endogenous agonist, glutamate. Using an assay designed to specifically measure heterodimer populations at the surface, however, we found that Q124R substitution decreased the propensity of mGlu4 to heterodimerize with mGlu2 and mGlu7. Our study is the first to extensively describe the extent and regulatory factors of RNA editing of mGlu4 mRNA transcripts. In addition, we have proposed a novel functional consequence of this editing event that provides insights regarding its effects in vivo and expands the regulatory capacity for mGlu receptors.
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Haubrich, Jordi, Joan Font, Robert B. Quast, Anne Goupil-Lamy, Pauline Scholler, Damien Nevoltris, Francine Acher, et al. "A nanobody activating metabotropic glutamate receptor 4 discriminates between homo- and heterodimers." Proceedings of the National Academy of Sciences 118, no. 33 (August 12, 2021): e2105848118. http://dx.doi.org/10.1073/pnas.2105848118.

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There is growing interest in developing biologics due to their high target selectivity. The G protein–coupled homo- and heterodimeric metabotropic glutamate (mGlu) receptors regulate many synapses and are promising targets for the treatment of numerous brain diseases. Although subtype-selective allosteric small molecules have been reported, their effects on the recently discovered heterodimeric receptors are often not known. Here, we describe a nanobody that specifically and fully activates homodimeric human mGlu4 receptors. Molecular modeling and mutagenesis studies revealed that the nanobody acts by stabilizing the closed active state of the glutamate binding domain by interacting with both lobes. In contrast, this nanobody does not activate the heterodimeric mGlu2-4 but acts as a pure positive allosteric modulator. These data further reveal how an antibody can fully activate a class C receptor and bring further evidence that nanobodies represent an alternative way to specifically control mGlu receptor subtypes.
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Zammataro, Magda, Santina Chiechio, Michael C. Montana, Anna Traficante, Agata Copani, Ferdinando Nicoletti, and Robert W. Gereau. "mGlu2 Metabotropic Glutamate Receptors Restrain Inflammatory Pain and Mediate the Analgesic Activity of Dual mGlu2/mGlu3 Receptor Agonists." Molecular Pain 7 (January 2011): 1744–8069. http://dx.doi.org/10.1186/1744-8069-7-6.

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Dissertations / Theses on the topic "MGlu2 receptor"

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Bossi, Simon. "Récepteurs présynaptiques métabotropiques du glutamate : études fonctionnelles au sein du système nerveux central de rongeur à l'aide de nouveaux outils pharmacologiques." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS488.

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Les récepteurs métabotropiques du glutamate (mGlus) sont connus pour moduler la transmission excitatrice dans le système nerveux central. Parmi ces récepteurs, ceux localisés au niveau de la pré-synapse, exercent un rôle d’autorécepteur, entrainant une diminution de la libération de glutamate à la suite de leur activation. L’étude du rôle fonctionnel de tel ou tel sous-type de mGlus est complexe compte-tenu du manque d’outils pharmacologiques sélectifs permettant de cibler spécifiquement un sous-type mGlus donné. Dans un premier temps, nous avons, par des techniques d’électrophysiologie et de fluorométrie calcique, validé de nouveaux outils pharmacologiques spécifiques de mGlu2 (un « nanobody » modulateur allostérique positif, PAM) et mGlu4 (OptoGluNAM4.1, un modulateur allostérique négatif, NAM), respectivement sur tranches d’hippocampe et de cervelet de rongeur. Nous avons ensuite, au sein du cortex cérébelleux, utilisé l’OptoGluNAM4.1 pour démontrer pour la première fois, l’implication de mGlu4 dans un contexte physio-pathologique: l’ischémie cérébelleuse. A l’aide d’outils pharmacologiques plus classiques nous avons également pu mettre en évidence, au sein des synapses qu’établissent les fibres parallèles avec les cellules de Purkinje l’existence d’un “dialogue” entre les récepteurs mGlu4 et les récepteurs A1 (récepteurs à l’adénosine de type 1), conséquence d’intéractions fonctionnelles entres les voies de signalisation de ces récepteurs présynaptiques dimériques et/ou conséquence de l’association physique de ces récepteurs au sein d’hétérodimères, fonctionnels
Metabotropic glutamate receptors (mGlus) are known to modulate excitatory transmission in the Central Nervous System. Among them, those situated at the pre-synaptic level behave like autoreceptors, their activation leading to a decrease in glutamate release. Functional studies of the different mGlus have been hampered by the lack of selective pharmacological tools specifically targeting a given subgroup of these receptors. As a first step, using electrophysiological and calcium fluorometry techniques, we validated new specific pharmacological tools acting on mGlu2 (a nanobody, positive allosteric modulator, PAM) and mGlu4 (OptoGluNAM4.1, a negative allosteric modulator, NAM) on rodent hippocampal and cerebellar slices, respectively. We then used the OptoGluNAM4.1 in the cerebellar cortex to demonstrate, for the first time, the involvement of mGlu4 in a physiopathological condition: cerebellar ischemia. Using more conventional pharmacological tools, we were also able to show the existence of a dialog between mGlu4 and A1 (Adenosine type 1) receptors at the level of the synapse between parallel fibers and Purkinje cells. Whether this dialog results from functional interactions between the signaling pathways of these pre-synaptic dimeric receptors and/or is a consequence of their physical association in heterodimers is presently under study
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Philibert, Clémentine. "Le récepteur métabotropique du glutamate mGlu2 interagit avec et transactive le récepteur tyrosine kinase TrkB : rôle dans la réponse comportementale aux antipsychotiques glutamatergiques." Thesis, Université de Montpellier (2022-….), 2022. http://www.theses.fr/2022UMONT019.

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La schizophrénie est un trouble mental débilitant multifactoriel affectant 1 % de la population mondiale qui est caractérisé par trois classes de symptômes : les symptômes positifs (hallucinations), les symptômes négatifs (isolement social) et les déficits cognitifs (altération de la mémoire de travail). Les antipsychotiques actuels tels que les antipsychotiques typiques et atypiques, ciblant respectivement le récepteur D2 de la dopamine et le récepteur 5-HT2A de la sérotonine, sont capables de traiter efficacement les symptômes positifs et peu efficaces contre les symptômes négatifs. Le récepteur métabotropique du glutamate mGlu2 (mGluR2) continue d'attirer une attention particulière compte tenu de son implication dans la schizophrénie. En effet, ce récepteur couplé aux protéines G (RCPG) est la cible principale d'une nouvelle génération d'antipsychotiques actuellement en essai clinique qui traite efficacement les trois classes de symptômes de la schizophrénie sans pour autant entraîner d’effets secondaires notables. Néanmoins, sa signalisation dans le cerveau et ses perturbations pathologiques restent mal caractérisées. En effet, la caractérisation spécifique de la signalisation native de mGluR2 est encore difficile en raison d'une forte homologie de séquences avec mGluR3, complexifiant la production de ligands ou d'anticorps spécifiques. Nous avons tiré parti d'un anticorps monocaténaire de lama (nanocorps) ciblant spécifiquement mGluR2 afin de purifier le récepteur endogène et ses interacteurs du cortex préfrontal de souris, une région cérébrale connue pour exprimer fortement mGluR2 mais également fortement perturbée dans la schizophrénie. Cet interactome a été caractérisé par spectrométrie de masse à haute résolution (AP-MS), et les annotations bioinformatiques des ontologies de gènes de ces partenaires protéiques ont révélé une grande pertinence pour les fonctions de mGluR2. L'un de ces interacteurs s'est révélé plus qu'attractif : le récepteur aux neurotrophines TrkB. Très significatif dans notre analyse AP-MS, il a été démontré que l'ARNm de TrkB est diminué dans le tissu cérébral des patients atteints de schizophrénie par rapport aux tissus témoins. Nous avons pu déterminer que : 1) mGluR2 et TrkB interagissent spécifiquement à une faible proximité, 2) cette interaction est modulée en fonction de leur état d'activation, 3) la stimulation de mGluR2 transactive TrkB dans les neurones corticaux dans le cortex préfrontal, 4) l'activation de TrkB conduit à la modulation de l'activité canonique de mGluR2 et 5) les effets antipsychotique des agonistes de mGluR2 dans un modèle préclinique de schizophrénie sont médiés par TrkB pour le sauvetage des déficits négatifs et cognitifs. En bref, cette transactivation réciproque de mGluR2 et TrkB est prometteuse puisque TrkB s’avère avoir un rôle central dans la médiation des effets antipsychotiques des ligands de mGluR2 dans les symptômes résistants jusqu'alors
Schizophrenia is a multifactorial debilitating mental disorder affecting 1 % of the world population characterized by three classes of symptoms: positive symptoms (e.g. hallucinations), negative symptoms (e.g. social isolation) and cognitive deficits (e.g. impaired working memory). Current antipsychotics such as typical and atypical antipsychotics, targeting dopamine D2 receptor and serotonin 5-HT2A receptor respectively, are able to treat efficiently the positive symptoms and partially the negative symptoms. However, antipsychotics treating efficiently the three classes of symptoms is still an unmet need. The metabotropic glutamate mGlu2 receptor (mGluR2) keeps on attracting particular attention given its implication in schizophrenia. This G protein-coupled receptor (GPCR) is the main target of a new generation of antipsychotics currently under clinical trial, treating efficiently the three class of symptoms without displaying any side effects. However, mGluR2 signaling in the brain and its pathological disturbances remain poorly characterized. Specific characterization of mGluR2 signaling in the brain was previously challenging due to a high homology of sequences with the structurally close metabotropic glutamate mGluR3 receptor, which complicated the production of specific ligands or antibodies. We have taken advantage of a single lama chain antibody (nanobody) specifically targeting mGluR2 in order to purify the endogenous receptor and its interacting proteins from mouse prefrontal cortex, a brain region known to strongly express mGluR2 but also highly disturbed in schizophrenia. This interactome was characterized by high resolution mass spectrometry and bioinformatics annotations of the gene ontologies of the candidate protein partners revealed high relevance to mGluR2 functions. One of these interactors revealed to be very attractive: the receptor tyrosine kinase TrkB. Highly significant in our AP-MS analysis, the mRNA of this rec eptor tyrosine kinase has been shown to be decreased in the brain tissue of patients with schizophrenia in comparison to control tissues. We were able to decipher that: 1) mGluR2 and TrkB interact specifically, 2) this interaction is modulated by the conformational state of both receptors, 3) mGluR2 stimulation by its agonist transactivates TrkB in cortical neurons in the prefrontal cortex, 4) the activation of TrkB leads to the modulation of the canonical activity of mGluR2 and 5) the antipsychotic-like effects of mGluR2 agonists in preclinical model of schizophrenia are mediated by TrkB for negative and cognitive deficits rescue. In summary, this reciprocal transactivation of mGluR2 and TrkB is highly promising and might have a pathophysiological influence in psychosis such as schizophrenia, but most importantly, TrkB has a pivotal role in mediating the antipsychotic-like effect of mGluR2 ligand for symptoms resisting so far to current antipsychotics
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Sharpe, Erica Frances. "Antinociception by systemic metabotropic glutamate receptor ligands." Thesis, University of Bristol, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368395.

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Bradley, Sophie Jane. "Regulation and pharmacological manipulation of the type 5 metabotropic glutamate (mGlu5) receptor." Thesis, University of Leicester, 2011. http://hdl.handle.net/2381/9391.

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Compelling evidence has emerged to indicate that astrocytes play crucial roles in neurotransmitter signalling, in addition to CNS homeostatic functions. Astrocytes can communicate with each other and with neurons, giving rise to the concept of the ‘tripartite synapse’. Expression of type 5 metabotropic glutamate (mGlu5) receptors in astrocytes is now well-established. Agonist stimulation of mGlu5 receptors initiates robust oscillatory changes in cytosolic Ca2+ concentration in single cells by rapid, repeated cycles of phosphorylation/dephosphorylation of the mGlu5 receptor, involving PKC and unidentified protein phosphatase activities in recombinant and native mGlu5 receptor-expressing systems. Each of the mGlu5 receptor positive allosteric modulators (PAMs) studied (DFB, CPPHA, CDPPB and ADX47273), failed to stimulate a Ca2+ response when applied alone, but increased the frequency of Ca2+ oscillations induced by glutamate or other orthosteric agonists. PAMs and negative allosteric modulators (NAMs) caused respectively graded increases and decreases in the Ca2+ oscillation frequency stimulated by orthosteric agonist. These data demonstrate that allosteric modulators can “tune” the Ca2+ oscillation frequency initiated by mGlu5 receptor activation and this might allow pharmacological modification of the downstream processes (e.g. transcriptional regulation) not achievable through orthosteric ligand interactions. Further investigation into the mechanism of action of PAMs revealed marked differences with respect to their modulation of orthosteric agonist affinity and efficacy. Thus, while DFB and CDPPB primarily exert their allosteric modulatory effects through modifying orthosteric agonist affinity, effects of ADX47273 are primarily mediated through an efficacy-driven modulation. Investigating the mechanisms underlying mGlu5 receptor-mediated Ca2+ oscillations in astrocytes has provided further evidence for the involvement of PKC(s) and protein phosphatase(s) in the rapid phosphorylation/dephosphorylation cycles occurring at the C-terminal of mGlu5 receptors, a process termed ‘dynamic uncoupling’. This work has been extended using specific siRNA knockdown to elucidate the potential PKC isoenzyme(s) that determine mGlu5 receptor regulation of Ca2+ oscillation frequency in astrocytes.
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Imre. "Group II metabotropic glutamate (mGlu2/3) receptors potential drug targets for the treatment of schizophrenia and anxiety? /." [S.l. : [Groningen : s.n.] ; University Library Groningen] [Host], 2006. http://irs.ub.rug.nl/ppn/297586998.

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Goyet, Elise. "Dynamique et fonction des interactions entre récepteurs du glutamate et de la dopamine." Thesis, Montpellier, 2017. http://www.theses.fr/2017MONTT019.

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Dans certaines aires cérébrales, l’action synergique du glutamate et de la dopamine est nécessaire pour induire et maintenir la plasticité synaptique. Un dialogue fonctionnel entre le récepteur métabotropique du glutamate mGlu5 et le récepteur de la dopamine D1 a été mise en évidence. Par ailleurs, de nombreuses études ont démontré que les récepteurs couplés aux protéines G ont la capacité de former des hétéromères créant ainsi de nouvelles entités fonctionnelles. En s’appuyant sur l’hypothèse d’une hétéromérisation des récepteurs, l’objectif de ce projet de thèse était d’étudier les mécanismes moléculaires qui sous-tendent une synergie fonctionnelle entre les récepteurs mGlu5 et D1. Dans la première partie de ce travail, j’ai caractérisé les bénéfices de la Nanoluciférase, une luciférase très lumineuse, pour améliorer la technique de BRET en imagerie (Bioluminescence Resonance Energy Transfer imaging) qui permet d’étudier la dynamique des interactions entre protéines dans les cellules vivantes. Les bénéfices mis en évidence en termes de résolution spatio-temporelle, de stabilité et de sensibilité du signal ont été exploités pour la suite de ce projet. Dans la seconde partie de ce travail, les améliorations techniques mentionnées ci-dessus ont permis de mettre en évidence pour la première fois des hétéromères mGlu5/D1 dans des neurones en culture. En outre, nous avons montré que la co-expression des récepteurs mGlu5 et D1 en système hétérologue favorise la signalisation calcique, d’une part en augmentant l'activité constitutive de mGlu5 et, d’autre part, en créant une voie de libération du calcium intracellulaire atypique induite par l'agoniste D1.Ces résultats apportent de nouveaux éléments de compréhension des bases moléculaires du dialogue fonctionnel glutamate/dopamine dans le contrôle de la communication neuronale en conditions physiologiques et ouvrent la voie à de nouvelles stratégies thérapeutiques capables de moduler sélectivement la fonction des hétéromères
In some specific brain areas, synergism between glutamate and dopamine transmission is required to induce synaptic plasticity. Metabotropic glutamate receptor mGlu5 and dopamine receptor D1 are both known to control synaptic plasticity. Moreover, multiple lines of evidence converge toward the ability of G-protein coupled receptors to form dynamic heteromers thereby creating new entities with unique properties. Focusing on the hypothesis of receptor heteromerization, my PhD project aimed at investigating the molecular mechanisms underlying a functional interplay between mGlu5 and D1 receptors.To address this issue, a first part of this work consisted in improving single-cell Bioluminescent Resonance Energy Transfer (BRET) imaging, a technology enabling to study real time protein-protein interaction dynamics in living cells. Using the Nanoluciferase, an extremely bright luciferase, we characterized a faster and higher resolution single-cell BRET imaging technique with unprecedented performance in terms of temporal and spatial resolution, duration of signal stability and signal sensitivity. In the second part of this project, we showed that mGlu5 and D1 can form heteromers in heterologous expression system. The above-mentioned improvements of single-cell BRET imaging technique allowed to evidence the occurrence and the dynamics of mGlu5/D1 heteromers in cultured primary neurons. Furthermore, our results showed that the co-expression of mGlu5 and D1 receptors modifies single receptor properties to favor calcium signaling by increasing mGlu5 constitutive activity and creating a D1 agonist-induced activation of Ca2+ release from intracellular stores.These findings advance our knowledge about the molecular basis of the glutamate/dopamine functional dialogue to control neuronal communication in physiological conditions. Further investigation will help the dissection of the mGlu5/D1 heteromer specific signaling pathway with the hope of defining new therapeutics that may selectively modulate heteromer function and thus bypass undesirable side effects
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Petersson, Marcus. "Beyond AMPA and NMDA: Slow synaptic mGlu/TRPC currents : Implications for dendritic integration." Licentiate thesis, KTH, Computational Biology, CB, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-24833.

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In order to understand how the brain functions, under normal as well as pathological conditions, it is important to study the mechanisms underlying information integration. Depending on the nature of an input arriving at a synapse, different strategies may be used by the neuron to integrate and respond to the input. Naturally, if a short train of high-frequency synaptic input arrives, it may be beneficial for the neuron to be equipped with a fast mechanism that is highly sensitive to inputs on a short time scale. If, on the contrary, inputs arriving with low frequency are to be processed, it may be necessary for the neuron to possess slow mechanisms of integration. For example, in certain working memory tasks (e. g. delay-match-to-sample), sensory inputs may arrive separated by silent intervals in the range of seconds, and the subject should respond if the current input is identical to the preceeding input. It has been suggested that single neurons, due to intrinsic mechanisms outlasting the duration of input, may be able to perform such calculations. In this work, I have studied a mechanism thought to be particularly important in supporting the integration of low-frequency synaptic inputs. It is mediated by a cascade of events that starts with activation of group I metabotropic glutamate receptors (mGlu1/5), and ends with a membrane depolarization caused by a current that is mediated by canonical transient receptor potential (TRPC) ion channels. This current, denoted ITRPC, is the focus of this thesis.

A specific objective of this thesis is to study the role of ITRPC in the integration of synaptic inputs arriving at a low frequency, < 10 Hz. Our hypothesis is that, in contrast to the well-studied, rapidly decaying AMPA and NMDA currents, ITRPC is well-suited for supporting temporal summation of such synaptic input. The reason for choosing this range of frequencies is that neurons often communicate with signals (spikes) around 8 Hz, as shown by single-unit recordings in behaving animals. This is true for several regions of the brain, including the entorhinal cortex (EC) which is known to play a key role in producing working memory function and enabling long-term memory formation in the hippocampus.

Although there is strong evidence suggesting that ITRPC is important for neuronal communication, I have not encountered a systematic study of how this current contributes to synaptic integration. Since it is difficult to directly measure the electrical activity in dendritic branches using experimental techniques, I use computational modeling for this purpose. I implemented the components necessary for studying ITRPC, including a detailed model of extrasynaptic glutamate concentration, mGlu1/5 dynamics and the TRPC channel itself. I tuned the model to replicate electrophysiological in vitro data from pyramidal neurons of the rodent EC, provided by our experimental collaborator. Since we were interested in the role of ITRPC in temporal summation, a specific aim was to study how its decay time constant (τdecay) is affected by synaptic stimulus parameters.

The hypothesis described above is supported by our simulation results, as we show that synaptic inputs arriving at frequencies as low as 3 - 4 Hz can be effectively summed. We also show that τdecay increases with increasing stimulus duration and frequency, and that it is linearly dependent on the maximal glutamate concentration. Under some circumstances it was problematic to directly measure τdecay, and we then used a pair-pulse paradigm to get an indirect estimate of τdecay.

I am not aware of any computational model work taking into account the synaptically evoked ITRPC current, prior to the current study, and believe that it is the first of its kind. We suggest that ITRPC is important for slow synaptic integration, not only in the EC, but in several cortical and subcortical regions that contain mGlu1/5 and TRPC subunits, such as the prefrontal cortex. I will argue that this is further supported by studies using pharmacological blockers as well as studies on genetically modified animals.


QC 20101005
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8

Reid, Morag. "Group I mGlu receptors : desensitization properties and modulation of cerebrocortical glutamate release." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311428.

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9

Younkin, Jason W. "Allosteric Effects of G-Protein Coupled Receptor Heteromerization: Relevance to Psychosis." VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4457.

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G-protein coupled receptors (GPCRs) implicated in disease are the predominant pharmaceutical targets. Growing evidence suggests that GPCRs form homo- and heteromeric complexes, resulting in allosteric functional changes. Ligands targeting one receptor can alter the function of the other receptor or receptors. Knowledge of these functional changes will provide unique opportunities to treat diseases. We examined two GPCR heteromers implicated in psychosis: mGlu2R-5HT2AR and D2R-5HT2AR. Using whole-cell patch clamp, we studied HEK-293 cells stably transfected with mGlu2R and 5HT2AR. Maximal heteromer formation allows inverse agonists to increase the G-protein activity of the opposite receptor, while sub-maximal heteromer formation does not. However, similar results are obtained in sub-maximal heteromer cells by applying a combination of a mGlu2R synthetic agonist with a 5HT2AR anti-psychotic drug. These results confirm our oocyte results, now in a mammalian cell line. Using two-electrode voltage clamp, we also investigated the allosteric changes upon heteromerization of D2R-5HT2AR in oocytes injected with appropriate cRNAs. Heteromer formation in the presence of dopamine or serotonin results in an increase in G-protein activity of each receptor while the simultaneous presence of both neurotransmitters further increases the G-protein activity. The addition of synthetic agonists or anti-psychotics decreases the G-protein activity of the opposite receptor while agonizing or antagonizing its target receptor, respectively. Maximal allosteric effects upon D2R-5HT2AR formation only occur at a specific cRNA injection ratio, but partial effects exist at other ratios. Our data suggest that allosteric functional changes upon heteromerization are physiologically relevant and are mostly different when comparing mGlu2R-5HT2AR to D2R-5HT2AR.
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Brown-Wright, Sian Heledd. "Investigating metabotropic glutamate receptor 5 (mGlu5) as a novel therapeutic target in motor neuron disease (MND)." Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/22583/.

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Books on the topic "MGlu2 receptor"

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Ngomba, Richard Teke, Giuseppe Di Giovanni, Giuseppe Battaglia, and Ferdinando Nicoletti, eds. mGLU Receptors. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56170-7.

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Giovanni, Giuseppe Di, Richard Teke Ngomba, Ferdinando Nicoletti, and Giuseppe Battaglia. mGLU Receptors. Humana, 2017.

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Giovanni, Giuseppe Di, Richard Teke Ngomba, Ferdinando Nicoletti, and Giuseppe Battaglia. MGLU Receptors. Springer International Publishing AG, 2018.

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Book chapters on the topic "MGlu2 receptor"

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Chaki, Shigeyuki. "mGlu2/3 Receptor Antagonists as Rapid-Acting Antidepressants." In Contemporary Clinical Neuroscience, 111–26. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-79790-4_7.

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Perry, Christina J., M. Foster Olive, and Andrew J. Lawrence. "mGlu5 Signaling: A Target for Addiction Therapeutics?" In mGLU Receptors, 1–14. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56170-7_1.

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Morin, Nicolas, and Thérèse Di Paolo. "mGlu5 Receptors in Parkinson’s Disease and MPTP-Lesioned Monkeys: Behavior and Brain Molecular Correlates." In mGLU Receptors, 183–205. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56170-7_10.

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van Luijtelaar, Gilles, Valerio D’Amore, Ines Santolini, and Richard T. Ngomba. "Is There a Future for mGlu5-Positive Allosteric Modulators in Absence Epilepsy? A Comparison with Ethosuximide." In mGLU Receptors, 207–24. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56170-7_11.

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Jia, Zhengping, and Graham Collingridge. "Regulation of Hippocampal mGluR-Dependent Long-Term Depression by GluA2-Dependent Cofilin-Mediated Actin Remodeling." In mGLU Receptors, 225–39. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56170-7_12.

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Ferraguti, Francesco. "Metabotropic Glutamate Receptors in Amygdala Functions." In mGLU Receptors, 241–77. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56170-7_13.

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Guida, Francesca, Enza Palazzo, Livio Luongo, Ida Marabese, Vito de Novellis, Sabatino Maione, and Francesco Rossi. "Supraspinal Metabotropic Glutamate Receptors: An Endogenous Substrate for Alleviating Chronic Pain and Related Affective Disorders." In mGLU Receptors, 15–31. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56170-7_2.

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Gubellini, Paolo, Liliya Iskhakova, Yoland Smith, and Marianne Amalric. "Metabotropic Glutamate Receptors and Parkinson’s Disease: Basic and Preclinical Neuroscience." In mGLU Receptors, 33–57. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56170-7_3.

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González-Maeso, Javier. "Metabotropic Glutamate 2 (mGlu2) Receptors and Schizophrenia Treatment." In mGLU Receptors, 59–78. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56170-7_4.

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Hagena, Hardy, and Denise Manahan-Vaughan. "mGlu5: A Metabotropic Glutamate Receptor at the Hub of Hippocampal Information Processing, Persistent Synaptic Plasticity, and Long-Term Memory." In mGLU Receptors, 79–101. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56170-7_5.

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Conference papers on the topic "MGlu2 receptor"

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Seyedbarhagh, Mahsasadat, Arash Ahmadi, and Majid Ahmadi. "Digital Realization for Ca2+ Waves Stimulated by the (mGlu5) Receptors." In 2021 International Symposium on Signals, Circuits and Systems (ISSCS). IEEE, 2021. http://dx.doi.org/10.1109/isscs52333.2021.9497380.

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Tayo, Lemmuel L., Alisha Marcelle C. Aquino, Andrea Matira, and Reincess Valbuena. "Computational analysis of the binding interactions of omega-conotoxins on GABAb and mGlu receptors." In ICBET 2022: 2022 12th International Conference on Biomedical Engineering and Technology. New York, NY, USA: ACM, 2022. http://dx.doi.org/10.1145/3535694.3535717.

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Gelb, Tara, Sergey Pshenichkin, Hannah A. Hathaway, Ewa Grajkowska, Barry B. Wolfe, and Jarda T. Wroblewski. "Abstract A15: mGlu1 Receptors and downstream signal transduction proteins as therapeutic targets for the treatment of metastatic melanoma." In Abstracts: AACR Special Conference on Advances in Melanoma: From Biology to Therapy; September 20-23, 2014; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.mel2014-a15.

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