Academic literature on the topic 'Glutamatergic receptors'

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Journal articles on the topic "Glutamatergic receptors"

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Crowder, Tara L., and Jeff L. Weiner. "Functional Characterization of Kainate Receptors in the Rat Nucleus Accumbens Core Region." Journal of Neurophysiology 88, no. 1 (2002): 41–48. http://dx.doi.org/10.1152/jn.2002.88.1.41.

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The nucleus accumbens, a brain region involved in motivation, attention, and reward, receives substantial glutamatergic innervation from many limbic structures. This excitatory glutamatergic input plays an integral role in both normal and pathophysiological states. Despite the importance of glutamatergic transmission in the nucleus accumbens, the specific receptor subtypes that mediate glutamatergic signaling in this brain region have not been fully characterized. The current study sought to examine the possible role of the kainate subclass of glutamate receptor in the nucleus accumbens. Kaina
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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 invest
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Alkondon, Manickavasagom, Edna F. R. Pereira, and Edson X. Albuquerque. "NMDA and AMPA Receptors Contribute to the Nicotinic Cholinergic Excitation of CA1 Interneurons in the Rat Hippocampus." Journal of Neurophysiology 90, no. 3 (2003): 1613–25. http://dx.doi.org/10.1152/jn.00214.2003.

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In the hippocampus, glutamatergic inputs to pyramidal neurons and interneurons are modulated by α7* and α3β4* nicotinic acetylcholine receptors (nAChRs), respectively, present in glutamatergic neurons. This study examines how nicotinic AMPA, and NMDA receptor nAChR activities are integrated to regulate the excitability of CA1 stratum radiatum (SR) interneurons in rat hippocampal slices. At resting membrane potentials and in the presence of extracellular Mg2+ (1 mM), nicotinic agonists triggered in SR interneurons excitatory postsynaptic currents (EPSCs) that had two components: one mediated by
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Tamminga, Carol. "Glutamatergic aspects of schizophrenia." British Journal of Psychiatry 174, S37 (1999): 12–15. http://dx.doi.org/10.1192/s0007125000293598.

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Almost all the neurons in the brain are influenced by the excitatory amino acid glutamate. Glutamatergic neurotransmission has been associated functionally with a number of physiological processes and with certain pathophysiological processes, including schizophrenia. Imaging studies provide indirect evidence that glutamate may be involved in schizophrenia. Positron emission tomography scanning has shown a correlation between positive symptoms of schizophrenia and abnormalities of glucose metabolism in components of the limbic system with the highest concentration of glutamate receptors. Studi
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Gasparini, Fabrizio, Thérèse Di Paolo, and Baltazar Gomez-Mancilla. "Metabotropic Glutamate Receptors for Parkinson's Disease Therapy." Parkinson's Disease 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/196028.

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Excessive glutamatergic signalling within the basal ganglia is implicated in the progression of Parkinson’s disease (PD) and inthe emergence of dyskinesia associated with long-term treatment with L-DOPA. There is considerable research focus on the discovery and development of compounds that modulate glutamatergic signalling via glutamate receptors, as treatments for PD and L-DOPA-induced dyskinesia (LID). Although initial preclinical studies with ionotropic glutamate receptor antagonists showed antiparkinsonian and antidyskinetic activity, their clinical use was limited due to psychiatric adve
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Espinosa, Felipe, and Ege T. Kavalali. "NMDA Receptor Activation by Spontaneous Glutamatergic Neurotransmission." Journal of Neurophysiology 101, no. 5 (2009): 2290–96. http://dx.doi.org/10.1152/jn.90754.2008.

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Under physiological conditions N-methyl-d-aspartate (NMDA) receptor activation requires coincidence of presynaptic glutamate release and postsynaptic depolarization due to the voltage-dependent block of these receptors by extracellular Mg2+. Therefore spontaneous neurotransmission in the absence of action potential firing is not expected to lead to significant NMDA receptor activation. Here we tested this assumption in layer IV neurons in neocortex at their resting membrane potential (approximately −67 mV). In long-duration stable recordings, we averaged a large number of miniature excitatory
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DANYSZ, W., and W. J. SCHMIDT. "GLUTAMATERGIC RECEPTORS AND LEARNING - METHODOLOGICAL ASPECTS." Behavioural Pharmacology 3, Supplement (1992): 6. http://dx.doi.org/10.1097/00008877-199204001-00014.

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Dasilva, Miguel, Christian Brandt, Marc Alwin Gieselmann, Claudia Distler, and Alexander Thiele. "Contribution of Ionotropic Glutamatergic Receptors to Excitability and Attentional Signals in Macaque Frontal Eye Field." Cerebral Cortex 31, no. 7 (2021): 3266–84. http://dx.doi.org/10.1093/cercor/bhab007.

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Abstract Top-down attention, controlled by frontal cortical areas, is a key component of cognitive operations. How different neurotransmitters and neuromodulators flexibly change the cellular and network interactions with attention demands remains poorly understood. While acetylcholine and dopamine are critically involved, glutamatergic receptors have been proposed to play important roles. To understand their contribution to attentional signals, we investigated how ionotropic glutamatergic receptors in the frontal eye field (FEF) of male macaques contribute to neuronal excitability and attenti
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Isaac, John TR, Roger A. Nicoll, and Robert C. Malenka. "Silent glutamatergic synapses in the mammalian brain." Canadian Journal of Physiology and Pharmacology 77, no. 9 (1999): 735–37. http://dx.doi.org/10.1139/y99-075.

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Excitatory synaptic transmission in the mammalian brain is mediated primarily by α-amino-3-hydroxy-5-methylisoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptors that are thought to be co-localized at individual synapses. However, recent electrophysiological and anatomical data suggest that the synaptic localization of AMPA and NMDA receptors may be independently regulated by neural activity. These data are reviewed here and the implications of these findings for the mechanisms underlying synaptic plasticity are discussed.Key words: glutamate receptor, long-term potentiation
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Mantilla, Carlos B., Heather M. Gransee, Wen-Zhi Zhan, and Gary C. Sieck. "Impact of glutamatergic and serotonergic neurotransmission on diaphragm muscle activity after cervical spinal hemisection." Journal of Neurophysiology 118, no. 3 (2017): 1732–38. http://dx.doi.org/10.1152/jn.00345.2017.

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Incomplete cervical spinal cord hemisection at C2 (SH) disrupts descending excitatory drive to phrenic motoneurons, paralyzing the ipsilateral diaphragm muscle. Spontaneous recovery over time is associated with increased phrenic motoneuron expression of glutamatergic N-methyl-d-aspartate (NMDA) and serotonergic 5-HT2A receptors. We hypothesized that NMDA and 5-HT2A receptor-mediated neurotransmission play a role in ipsilateral diaphragm muscle activity post-SH. Adult male Sprague-Dawley rats were implanted with bilateral diaphragm EMG electrodes for chronic EMG recordings up to 28 days post-SH
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Dissertations / Theses on the topic "Glutamatergic receptors"

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Hammond, Victoria. "α7 nicotinic acetylcholine receptors at the glutamatergic synapse". Thesis, University of Bath, 2014. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.633163.

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Nicotinic acetylcholine receptor (nAChR) activation is neuroprotective and nicotine is a cognitive enhancer. Loss of nAChRs, deposition of tau neurofibrillary tangles, cleavage of amyloid precursor protein (APP) and inflammation are well documented in the pathogenesis of Alzheimer’s disease (AD). Sequential cleavage of APP by β- and γ-secretase enzymes generates soluble Aβ peptides, with oligomeric forms of Aβ implicated in both the control of synaptic excitability and dysregulation of synaptic transmission and induction of neuronal death in AD. Aβ production is inhibited by calcium-dependent
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Braithwaite, Steven P. "Investigation of the function, pharmacology and cell biology of kainate receptors." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302064.

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Nilsson, Linda K. "Glutamatergic mechanisms in schizophrenia: role of endogenous kynurenic acid /." Stockholm : Dept. of Physiology and Pharmacology, Karolinska institutet, 2005. http://diss.kib.ki.se/2005/91-7140-538-0/.

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Jezequel, Julie. "Impact of psychotomimetic molecules on glutamatergic N-Methyl-D-Aspartate receptors surface trafficking." Thesis, Bordeaux, 2016. http://www.theses.fr/2016BORD0232/document.

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Les récepteurs glutamatergiques de type N-Méthyl-D-Aspartate (RNMDA) jouent un rôle majeur dans de nombreux processus physiologiques, et leur implication dans la physiopathologie de certains troubles neuropsychiatriques tels que la schizophrénie est suggérée par un robuste faisceau de données cliniques et précliniques. Cependant, les mécanismes cellulaires et moléculaires conduisant à une telle dérégulation des RNMDA restent inexpliqués. La diffusion membranaire, mécanisme de contrôle spatial et temporel de la distribution des RNMDA à la surface des neurones, constitue un puissant régulateur d
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Konradsson, Åsa. "Modulation of prefrontal glutamatergic transmission and "atypicality" of antipsychotic drugs /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-344-3/.

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

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MARCHETTI, NATALIA. "THE DEVELOPMENT OF THE GLUTAMATERGIC NEURONS IS SHAPED BY IL-1BETA." Doctoral thesis, Università degli Studi di Milano, 2018. http://hdl.handle.net/2434/548638.

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The developing brain is exquisitely sensitive to immune system activation that, shaping the organism’s response to infections, may impact the development of the nervous system increasing susceptibility to behavioural and neurological diseases later in life. Experimental studies, in particular, link dysregulated production of pro-inflammatory cytokines (i.e. IL6 and IL-1β) to the onset of neurodevelopmental diseases later in life. Neonatal immune activation, through cytokines production, can have direct long-term effects on neuronal function by interfering with neurotransmitter function,
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Lee, Junyoung. "FURTHERING PHARMACOLOGICAL AND PHYSIOLOGICAL ASSESSMENT OF THE GLUTAMATERGIC RECEPTORS AT THE DROSOPHILA NEUROMUSCULAR JUNCTION." UKnowledge, 2009. http://uknowledge.uky.edu/gradschool_theses/619.

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Drosophila larval neuromuscular junctions (NMJs) serve as a model for synaptic physiology. The molecular sequence of the postsynaptic glutamate receptors has been described; however, the pharmacological profile has not been fully elucidated. Despite the postsynaptic molecular sequence used to classify the receptors as a kainate subtype, they do not respond pharmacologically as such. Kainate does not depolarize the muscle, but dampens evoked EPSP amplitudes. Quantal responses show a decreased amplitude and area under the voltage curve indicative of reduced postsynaptic receptor sensitivity to g
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Sacchi, Federico. "Glutamatergic Regulation of Adult Goldfish Radial Glial Cells Via Group III Metabotropic Glutamate Receptors." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/38535.

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Aromatase is an enzyme that converts androgens to estrogens. In teleosts, brain aromatase, also known as aromatase B (cy19a1b), is only expressed in radial glial cells (RGCs). This is in contrast to aromatase A, which is expressed in gonads. Estrogens such as estradiol (E2) modulate neurogenesis in the adult teleost brain. Recent studies show that E2 also differentially regulates aromatase B expression in goldfish RGCs. As a result, teleost RGCs are suggested to be involved in regulating neurogenesis. In addition, aromatase B expression in goldfish RGC is under the control of dopamine suggesti
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Ng, Ka-pak, and 吳嘉白. "Glutamatergic and GABAergic transmission regulate the maturation of vestibular circuitry for spatial recognition." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45200312.

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Books on the topic "Glutamatergic receptors"

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Turesson, Jenny. Oxygen chemoreflexes in fish with emphasis on Glutamatergic control mechanisms in the Medulla. Göteborg University, 2006.

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Kaar, Stephen J., Steven Potkin, and Oliver Howes. The neurobiology of antipsychotic treatment response and resistance. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198828761.003.0005.

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Dopamine D2/3 receptor occupancy by antipsychotic drugs is central to clinical response and many of their side effects. Yet the locus of dopaminergic alterations in the majority of patients with schizophrenia is not the D2/3 receptor but, instead, presynaptic, comprising elevated striatal dopamine synthesis and release capacity. However, whilst this explains why dopamine D2/3 receptor blockade is effective in many patients, a proportion of patients does not respond. In some this is because of inadequate antipsychotic blockade of dopamine receptors, but there are others who do not respond to an
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Henter, Ioline D., and Rodrigo Machado-Vieira. Novel therapeutic targets for bipolar disorder. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0030.

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The long-term course of bipolar disorder (BD) comprises recurrent depressive episodes and persistent residual symptoms for which standard therapeutic options are scarce and often ineffective. Glutamate is the major excitatory neurotransmitter in the central nervous system, and glutamate and its cognate receptors have consistently been implicated in the pathophysiology of mood disorders and in the development of novel therapeutics for these disorders. Since the rapid and robust antidepressant effects of the N-methyl-D-aspartate (NMDA) antagonist ketamine were first observed in 2000, other NMDA
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Geracioti, Thomas D., Jeffrey R. Strawn, and Matthew D. Wortman. Mechanisms of Action in the Pharmacology of PTSD. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0020.

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This chapter reviews medications currently available for PTSD in the context of their mechanisms of action, pathophysiological relevance, and clinical efficacy data. It systematically reviews aminergic mechanisms in PTSD pharmacology, including commonly used serotonin and norepinephrine agents, selective reuptake inhibitors and receptors drugs, as well as dopaminergic agents and psychostimulants. It also discusses the use of anticonvusants and antianxiety agents that modulate GABAergic and glutamatergic signaling, such as carbamazepine, VPA, benzodiazepines, gabapentine, and others. It also re
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Beninger, Richard J. Life's rewards. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198824091.001.0001.

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Life’s Rewards: Linking Dopamine, Incentive Learning, Schizophrenia, and the Mind explains how increased brain dopamine produces reward-related incentive learning, the acquisition by neutral stimuli of increased ability to elicit approach and other responses. Dopamine decreases may produce inverse incentive learning, the loss by stimuli of the ability to elicit approach and other responses. Incentive learning is gradually lost when dopamine receptors are blocked. The brain has multiple memory systems defined as “declarative” and “non-declarative;” incentive learning produces one form of non-de
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Marques, Tiago Reis, and Shitij Kapur. Novel Approaches for Treating Psychotic Disorders. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0021.

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Current antipsychotic medications have been the mainstay in the treatment of schizophrenia since chlorpromazine was introduced in 1952. However, all antipsychotics share the same mechanism of action, which involves a blockade of the dopamine D2-receptor. This chapter covers recent attempts to develop new treatments for psychotic disorders. These include new approaches to the delivery of existing antipsychotic medications and the most recent and promising mechanisms of action that are distinct from existing antipsychotics. Some of the new mechanisms of action include drugs targeting the glutama
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Beninger, Richard J. Mechanisms of dopamine-mediated incentive learning. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198824091.003.0012.

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Mechanisms of dopamine-mediated incentive learning explains how sensory events, resulting from an animal’s movement and the environment, activate cortical glutamatergic projections to dendritic spines of striatal medium spiny neurons to initiate a wave of phosphorylation. If no rewarding stimulus is encountered, a subsequent wave of phosphatase activity undoes the phosphorylation. If a rewarding stimulus is encountered, dopamine initiates a cascade of events in D1 receptor-expressing medium spiny neurons that may prevent the phosphatase effects and work synergistically with signaling events pr
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Book chapters on the topic "Glutamatergic receptors"

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Tomita, Susumu. "Glutamatergic Pathways and Receptors." In Essentials of Cerebellum and Cerebellar Disorders. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-24551-5_29.

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Cepeda, Carlos, Véronique M. André, Emily L. Jocoy, and Michael S. Levine. "Dopamine Receptor Modulation of Glutamatergic Neurotransmission." In The Dopamine Receptors. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-333-6_11.

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Ascher, P. "Glutamate Receptors and Glutamatergic Synapses." In Receptors, Membrane Transport and Signal Transduction. Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74200-2_12.

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Sampedro, A., E. Tarragón, J. E. Yuste, et al. "Glutamatergic Receptors in Parkinson’s Disease." In Handbook of Neurotoxicity. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-5836-4_154.

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Williams, Stephen H., and Daniel Johnston. "Muscarinic Cholinergic Inhibition of Glutamatergic Transmission." In Presynaptic Receptors in the Mammalian Brain. Birkhäuser Boston, 1993. http://dx.doi.org/10.1007/978-1-4684-6825-0_3.

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Verkhratsky, Alexei, and Geoffrey Burnstock. "Purinergic and Glutamatergic Receptors on Astroglia." In Glutamate and ATP at the Interface of Metabolism and Signaling in the Brain. Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-08894-5_4.

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Shen, Weixing, and D. James Surmeier. "Dopaminergic Modulation of Glutamatergic Signaling in Striatal Medium Spiny Neurons." In The Dopamine Receptors. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-333-6_7.

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Frotscher, M., K. Mews, and G. Adelmann. "Morphological Characteristics of Glutamatergic Synapses in the Hippocampus." In Ionotropic Glutamate Receptors in the CNS. Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-662-08022-1_10.

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Calì, Corrado, Julie Marchaland, Osvaldo Mirante, and Paola Bezzi. "Chemokines as Neuromodulators: Regulation of Glutamatergic Transmission by CXCR4-Mediated Glutamate Release From Astrocytes." In Chemokine Receptors and NeuroAIDS. Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0793-6_12.

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Trussell, L. O. "Physiology of Glutamatergic Transmission at Calyceal and Endbulb Synapses of the Central Auditory Pathway." In Ionotropic Glutamate Receptors in the CNS. Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-662-08022-1_12.

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Conference papers on the topic "Glutamatergic receptors"

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Dumas, Sébastien J., Frédéric Perros, Gilles Bru-Mercier, et al. "LSC Abstract – Glutamatergic signaling through pulmonary vascular NMDA receptors in pulmonary hypertension." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa4898.

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Bouteiller, Jean-Marie C., Sushmita L. Allam, Nicolas Ambert, et al. "Influence of ionotropic receptors localization on glutamatergic synaptic response to paired-pulse stimulation protocol." In 2013 35th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2013. http://dx.doi.org/10.1109/embc.2013.6609681.

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Gabrielli, Ângelo, Camila Sousa Bragunce Alves, Bruna Oliveira Bicalho, and Débora Pimenta Alves. "Benefits and Challenges of Cannabis Use in the Treatment of Refractory Epilepsy." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.239.

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Introduction: Refractory epilepsy (RE) is a disease that causes continuous and debilitating seizures. Due to the ineffectiveness of antiepileptic therapies, there is a growing interest in drugs made with cannabidiol (CBD), a substance extracted from Cannabis. Objective: To point out benefits and challenges of the use of CBD in the treatment of RE. Methods: Literature review performed at PubMed, with the descriptors Epilepsy, Drug Therapy and Cannabis. Results: It is suggested that CBD is mediated by cannabinoid receptors coupled to protein G, by blockade of NMDA receptors, by GABAergic modulat
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Elói, Daniel Vinicius, Daniel Lopes Marques de Araújo, Gabriela Fonseca Marçal, Luana Soares Vargas, Matheus Garcia Ribeiro, and Nicollas Nunes Rabelo. "Canabinoids as a therapeutic alternative in refractory epilepsy." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.554.

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Introduction: Epilepsy is characterized by abnormal electrical discharges in the brain that generate neuronal hyperexcitability and hypersynchrony. In the last years, pharmacological strategies have been efficient in the control of epileptic seizures of approximately 80% of patients, however, there are still refractory cases. Objective: To elucidate new forms of epilepsy treatment with cannabinoids. Design: Systematic Review performed at Centro Universitário Atenas – Paracatu – Minas Gerais. Methods: Literature review performed in the SciELO and PubMed databases, with the following terms: epil
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Cruz, Leonardo Cardoso, Luis Gustavo Fraga Belotto, Sofia Dias Campos Machado, and Fabrício de Araújo Moreira. "Possible mechanisms of action of cannabidiol in the epilepsies: a review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.045.

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Background: Cannabidiol (CBD) is a compound of Cannabis Sativa plant that has been studied since the 1970s for its effectiveness in the treatment of refractory epilepsies. With the discovery of the endocannabinoid system, most recent studies have been dedicated to elucidating its mechanisms of action. Objective: To review scientific articles in order to enlightening the antiepileptic cannabidiol’s mechanisms of action. Methods: Literature review on both PubMed and Google Scholar searching for the terms: “epilepsy”, “cannabidiol” and “mechanism of action”. Results: We found that cannabidiol has
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Allam, Sushmita L., J. C. Bouteiller, Eric Y. Hu, et al. "Influence of ionotropic receptor location on their dynamics at glutamatergic synapses." In 2012 34th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2012. http://dx.doi.org/10.1109/embc.2012.6346194.

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"The role of insulin receptor signaling in regulation of synaptic glutamatergic hippocampal neurotransmission." In Bioinformatics of Genome Regulation and Structure/Systems Biology (BGRS/SB-2022) :. Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, 2022. http://dx.doi.org/10.18699/sbb-2022-486.

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Mohan, Ashwin, Sandeep Pendyam, Bradley C. Enke, Peter Kalivas, and Satish S. Nair. "Stochastic Model of Glutamatergic PFC-NAc Synapse Predicts Cocaine-Induced Changes in Receptor Occupancy." In ASME 2009 Dynamic Systems and Control Conference. ASMEDC, 2009. http://dx.doi.org/10.1115/dscc2009-2615.

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Neurotransmitter homeostasis in and around synapses involves random processes such as diffusion, molecular binding and unbinding. A three-dimensional stochastic diffusion model of a synapse was developed to provide molecular level details of neurotransmitter homeostasis not predicted by alternative models based on continuum approaches. This framework was used to estimate effective diffusion and provide a more accurate prediction of geometric tortuosity in the perisynaptic region. The stochastic model was used to predict the relative contributions of non-synaptic sources to extracellular concen
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Gómez-Carreño, Carlos Rodríguez, Antonio Ramírez García, Luis Beato Fernández, Irene Díaz Quero, and Estefanía Segura Escobar. "Craving and Priming of alcohol in depressive disorders. Bibliographic review and new therapies." In 22° Congreso de la Sociedad Española de Patología Dual (SEPD) 2020. SEPD, 2020. http://dx.doi.org/10.17579/sepd2020p140.

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Acute alcohol consumption produces positive reinforcement effects, through activation of brain reward circuit, includes limbic system structures (accumbens system and hippocampus). The comorbidity of depressive episode and alcohol abuse makes it necessary to propose new strategies for the treatment of this frequent clinical situation. We conducted a literature review of the combined treatments for major depressive disorder (MDD) with alcohol abuse. We review current literature on the use of new treatments in alcohol consumption with pattern of abuse (binge drinking). Recent studies support the
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Kaczmarczyk, Michael, Katja Wingenfeld, Jan Nowacki, et al. "Mineralocorticoid and glutamatergic NMDA receptor stimulation does not influence spatial learning and memory in depressed individuals and healthy control." In Abstracts of the 3rd Symposium of the Arbeitsgemeinschaft für Neuropsychopharmakologie und Pharmakopsychiatrie (AGNP) and Deutsche Gesellschaft für Biologische Psychiatrie (DGBP). Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0042-1757660.

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