Relevant bibliographies by topics / AMPA

Academic literature on the topic 'AMPA'

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Published: 4 June 2021
Last updated: 21 February 2023

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Journal articles on the topic "AMPA"

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Kampstra, Arieke Suzanna Berendina, Jacqueline Stephanie Dekkers, Mikhail Volkov, Annemarie L. Dorjée, Lise Hafkenscheid, Ayla C. Kempers, Myrthe van Delft, et al. "Different classes of anti-modified protein antibodies are induced on exposure to antigens expressing only one type of modification." Annals of the Rheumatic Diseases 78, no. 7 (May 31, 2019): 908–16. http://dx.doi.org/10.1136/annrheumdis-2018-214950.

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ObjectivesAutoantibodies against post-translationally modified proteins (anti-modified protein antibodies or AMPAs) are a hallmark of rheumatoid arthritis (RA). A variety of classes of AMPAs against different modifications on proteins, such as citrullination, carbamylation and acetylation, have now been described in RA. At present, there is no conceptual framework explaining the concurrent presence or mutual relationship of different AMPA responses in RA. Here, we aimed to gain understanding of the co-occurrence of AMPA by postulating that the AMPA response shares a common ‘background’ that can evolve into different classes of AMPAs.MethodsMice were immunised with modified antigens and analysed for AMPA responses. In addition, reactivity of AMPA purified from patients with RA towards differently modified antigens was determined.ResultsImmunisation with carbamylated proteins induced AMPAs recognising carbamylated proteins and also acetylated proteins. Similarly, acetylated proteins generated (autoreactive) AMPAs against other modifications as well. Analysis of anti-citrullinated protein antibodies from patients with RA revealed that these also display reactivity to acetylated and carbamylated antigens. Similarly, anti-carbamylated protein antibodies showed cross-reactivity against all three post-translational modifications.ConclusionsDifferent AMPA responses can emerge from exposure to only a single type of modified protein. These findings indicate that different AMPA responses can originate from a common B-cell response that diversifies into multiple distinct AMPA responses and explain the presence of multiple AMPAs in RA, one of the hallmarks of the disease.
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Gainey, Melanie A., Vedakumar Tatavarty, Marc Nahmani, Heather Lin, and Gina G. Turrigiano. "Activity-dependent synaptic GRIP1 accumulation drives synaptic scaling up in response to action potential blockade." Proceedings of the National Academy of Sciences 112, no. 27 (June 24, 2015): E3590—E3599. http://dx.doi.org/10.1073/pnas.1510754112.

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Synaptic scaling is a form of homeostatic plasticity that stabilizes neuronal firing in response to changes in synapse number and strength. Scaling up in response to action-potential blockade is accomplished through increased synaptic accumulation of GluA2-containing AMPA receptors (AMPAR), but the receptor trafficking steps that drive this process remain largely obscure. Here, we show that the AMPAR-binding protein glutamate receptor-interacting protein-1 (GRIP1) is essential for regulated synaptic AMPAR accumulation during scaling up. Synaptic abundance of GRIP1 was enhanced by activity deprivation, directly increasing synaptic GRIP1 abundance through overexpression increased the amplitude of AMPA miniature excitatory postsynaptic currents (mEPSCs), and shRNA-mediated GRIP1 knockdown prevented scaling up of AMPA mEPSCs. Furthermore, knockdown and replace experiments targeting either GRIP1 or GluA2 revealed that scaling up requires the interaction between GRIP1 and GluA2. Finally, GRIP1 synaptic accumulation during scaling up did not require GluA2 binding. Taken together, our data support a model in which activity-dependent trafficking of GRIP1 to synaptic sites drives the forward trafficking and enhanced synaptic accumulation of GluA2-containing AMPAR during synaptic scaling up.
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Kalappa, Bopanna I., Charles T. Anderson, Jacob M. Goldberg, Stephen J. Lippard, and Thanos Tzounopoulos. "AMPA receptor inhibition by synaptically released zinc." Proceedings of the National Academy of Sciences 112, no. 51 (December 8, 2015): 15749–54. http://dx.doi.org/10.1073/pnas.1512296112.

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The vast amount of fast excitatory neurotransmission in the mammalian central nervous system is mediated by AMPA-subtype glutamate receptors (AMPARs). As a result, AMPAR-mediated synaptic transmission is implicated in nearly all aspects of brain development, function, and plasticity. Despite the central role of AMPARs in neurobiology, the fine-tuning of synaptic AMPA responses by endogenous modulators remains poorly understood. Here we provide evidence that endogenous zinc, released by single presynaptic action potentials, inhibits synaptic AMPA currents in the dorsal cochlear nucleus (DCN) and hippocampus. Exposure to loud sound reduces presynaptic zinc levels in the DCN and abolishes zinc inhibition, implicating zinc in experience-dependent AMPAR synaptic plasticity. Our results establish zinc as an activity-dependent, endogenous modulator of AMPARs that tunes fast excitatory neurotransmission and plasticity in glutamatergic synapses.
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Mao, Xia, Xinglong Gu, and Wei Lu. "GSG1L regulates the strength of AMPA receptor-mediated synaptic transmission but not AMPA receptor kinetics in hippocampal dentate granule neurons." Journal of Neurophysiology 117, no. 1 (January 1, 2017): 28–35. http://dx.doi.org/10.1152/jn.00307.2016.

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GSG1L is an AMPA receptor (AMPAR) auxiliary subunit that regulates AMPAR trafficking and function in hippocampal CA1 pyramidal neurons. However, its physiological roles in other types of neurons remain to be characterized. Here, we investigated the role of GSG1L in hippocampal dentate granule cells and found that GSG1L is important for the regulation of synaptic strength but is not critical for the modulation of AMPAR deactivation and desensitization kinetics. These data demonstrate a neuronal type-specific role of GSG1L and suggest that physiological function of AMPAR auxiliary subunits may vary in different types of neurons. NEW & NOTEWORTHY GSG1L is a newly identified AMPA receptor (AMPAR) auxiliary subunit and plays a unique role in the regulation of AMPAR trafficking and function in hippocampal CA1 pyramidal neurons. However, its role in the regulation of AMPARs in hippocampal dentate granule cells remains to be characterized. The current work reveals that GSG1L regulates strength of AMPAR-mediated synaptic transmission but not the receptor kinetic properties in hippocampal dentate granule neurons.
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Hanley, J. G. "Molecular mechanisms for regulation of AMPAR trafficking by PICK1." Biochemical Society Transactions 34, no. 5 (October 1, 2006): 931–35. http://dx.doi.org/10.1042/bst0340931.

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AMPA (α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) receptor trafficking is a fundamental mechanism for regulating synaptic strength, and hence may underlie cellular processes involved in learning and memory. PICK1 (protein that interacts with protein C-kinase) has recently emerged as a key regulator of AMPAR (AMPA receptor) traffic, and the precise molecular mechanisms of PICK1's action are just beginning to be unravelled. In this review, I summarize recent findings that describe some important molecular characteristics of PICK1 with respect to AMPAR cell biology.
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Morrell, Craig N., Henry Sun, Masahiro Ikeda, Jean-Claude Beique, Anne Marie Swaim, Emily Mason, Tanika V. Martin, et al. "Glutamate mediates platelet activation through the AMPA receptor." Journal of Experimental Medicine 205, no. 3 (February 18, 2008): 575–84. http://dx.doi.org/10.1084/jem.20071474.

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Glutamate is an excitatory neurotransmitter that binds to the kainate receptor, the N-methyl-D-aspartate (NMDA) receptor, and the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor (AMPAR). Each receptor was first characterized and cloned in the central nervous system (CNS). Glutamate is also present in the periphery, and glutamate receptors have been identified in nonneuronal tissues, including bone, heart, kidney, pancreas, and platelets. Platelets play a central role in normal thrombosis and hemostasis, as well as contributing greatly to diseases such as stroke and myocardial infarction. Despite the presence of glutamate in platelet granules, the role of glutamate during hemostasis is unknown. We now show that activated platelets release glutamate, that platelets express AMPAR subunits, and that glutamate increases agonist-induced platelet activation. Furthermore, we demonstrate that glutamate binding to the AMPAR increases intracellular sodium concentration and depolarizes platelets, which are important steps in platelet activation. In contrast, platelets treated with the AMPAR antagonist CNQX or platelets derived from GluR1 knockout mice are resistant to AMPA effects. Importantly, mice lacking GluR1 have a prolonged time to thrombosis in vivo. Our data identify glutamate as a regulator of platelet activation, and suggest that the AMPA receptor is a novel antithrombotic target.
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Wei, Mengping, Jian Zhang, Moye Jia, Chaojuan Yang, Yunlong Pan, Shuaiqi Li, Yiwen Luo, et al. "α/β-Hydrolase domain-containing 6 (ABHD6) negatively regulates the surface delivery and synaptic function of AMPA receptors." Proceedings of the National Academy of Sciences 113, no. 19 (April 25, 2016): E2695—E2704. http://dx.doi.org/10.1073/pnas.1524589113.

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In the brain, AMPA-type glutamate receptors are major postsynaptic receptors at excitatory synapses that mediate fast neurotransmission and synaptic plasticity. α/β-Hydrolase domain-containing 6 (ABHD6), a monoacylglycerol lipase, was previously found to be a component of AMPA receptor macromolecular complexes, but its physiological significance in the function of AMPA receptors (AMPARs) has remained unclear. The present study shows that overexpression of ABHD6 in neurons drastically reduced excitatory neurotransmission mediated by AMPA but not by NMDA receptors at excitatory synapses. Inactivation of ABHD6 expression in neurons by either CRISPR/Cas9 or shRNA knockdown methods significantly increased excitatory neurotransmission at excitatory synapses. Interestingly, overexpression of ABHD6 reduced glutamate-induced currents and the surface expression of GluA1 in HEK293T cells expressing GluA1 and stargazin, suggesting a direct functional interaction between these two proteins. The C-terminal tail of GluA1 was required for the binding between of ABHD6 and GluA1. Mutagenesis analysis revealed a GFCLIPQ sequence in the GluA1 C terminus that was essential for the inhibitory effect of ABHD6. The hydrolase activity of ABHD6 was not required for the effects of ABHD6 on AMPAR function in either neurons or transfected HEK293T cells. Thus, these findings reveal a novel and unexpected mechanism governing AMPAR trafficking at synapses through ABHD6.
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Barkóczi, Balázs, Gábor Juhász, Robert G. Averkin, Imre Vörös, Petra Vertes, Botond Penke, and Viktor Szegedi. "GluA1 Phosphorylation Alters Evoked Firing PatternIn Vivo." Neural Plasticity 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/286215.

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AMPA and NMDA receptors convey fast synaptic transmission in the CNS. Their relative contribution to synaptic output and phosphorylation state regulate synaptic plasticity. The AMPA receptor subunit GluA1 is central in synaptic plasticity. Phosphorylation of GluA1 regulates channel properties and trafficking. The firing rate averaged over several hundred ms is used to monitor cellular input. However, plasticity requires the timing of spiking within a few ms; therefore, it is important to understand how phosphorylation governs these events. Here, we investigate whether the GluA1 phosphorylation (p-GluA1) alters the spiking patterns of CA1 cellsin vivo. The antidepressant Tianeptine was used for inducing p-GluA1, which resulted in enhanced AMPA-evoked spiking. By comparing the spiking patterns of AMPA-evoked activity with matched firing rates, we show that the spike-trains after Tianeptine application show characteristic features, distinguishing from spike-trains triggered by strong AMPA stimulation. The interspike-interval distributions are different between the two groups, suggesting that neuronal output may differ when new inputs are activated compared to increasing the gain of previously activated receptors. Furthermore, we also show that NMDA evokes spiking with different patterns to AMPA spike-trains. These results support the role of the modulation of NMDAR/AMPAR ratio and p-GluA1 in plasticity and temporal coding.
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Myme, Chaelon I. O., Ken Sugino, Gina G. Turrigiano, and Sacha B. Nelson. "The NMDA-to-AMPA Ratio at Synapses Onto Layer 2/3 Pyramidal Neurons Is Conserved Across Prefrontal and Visual Cortices." Journal of Neurophysiology 90, no. 2 (August 2003): 771–79. http://dx.doi.org/10.1152/jn.00070.2003.

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To better understand regulation of N-methyl-d-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor complements across the cortex, and to investigate NMDA receptor (NMDAR)-based models of persistent activity, we compared NMDA/AMPA ratios in prefrontal (PFC) and visual cortex (VC) in rat. Whole cell voltage-clamp responses were recorded in brain slices from layer 2/3 pyramidal cells of the medial PFC and VC of rats aged p16–p21. Mixed miniature excitatory postsynaptic currents (mEPSCs) having AMPA receptor (AMPAR)- and NMDAR-mediated components were isolated in nominally 0 Mg2+ ACSF. Averaged mEPSCs were well-fit by double exponentials. No significant differences in the NMDA/AMPA ratio (PFC: 27 ± 1%; VC: 28 ± 3%), peak mEPSC amplitude (PFC: 19.1 ± 1 pA; VC: 17.5 ± 0.7 pA), NMDAR decay kinetics (PFC: 69 ± 8 ms; VC: 67 ± 6 ms), or degree of correlation between NMDAR- and AMPAR-mediated mEPSC components were found between the areas (PFC: n = 27; VC: n = 28). Recordings from older rats (p26–29) also showed no differences. EPSCs were evoked extracellularly in 2 mM Mg2+ at depolarized potentials; although the average NMDA/AMPA ratio was larger than that observed for mEPSCs, the ratio was similar in the two regions. In nominally 0 Mg2+ and in the presence of CNQX, spontaneous activation of NMDAR increased recording noise and produced a small tonic depolarization which was similar in both areas. We conclude that this basic property of excitatory transmission is conserved across PFC and VC synapses and is therefore unlikely to contribute to differences in firing patterns observed in vivo in the two regions.
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Rawal, Bijal, and Klaus Ballanyi. "Mediation of Sinusoidal Network Oscillations in the Locus Coeruleus of Newborn Rat Slices by Pharmacologically Distinct AMPA and KA Receptors." Brain Sciences 12, no. 7 (July 19, 2022): 945. http://dx.doi.org/10.3390/brainsci12070945.

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Brain control by locus coeruleus (LC) neurons involves afferent glutamate (Glu) inputs. In newborns, LC Glu receptors and responses may be sparse due to immaturity of the brain circuits providing such input. However, we reported, using newborn rat brain slices, that Glu and its ionotropic receptor (iGluR) agonist NMDA transform spontaneous local field potential (LFP) rhythm. Here, we studied whether α-amino-3-hydroxy-5-methyl-4-isoxazole propionic-acid (AMPA) and kainate (KA) iGluR subtypes also transform the LFP pattern. AMPA (0.25–0.5 µM) and KA (0.5–2.5 µM) merged ~0.2 s-lasting bell-shaped LFP events occurring at ~1 Hz into ~40% shorter and ~4-fold faster spindle-shaped and more regular sinusoidal oscillations. The AMPA/KA effects were associated with a 3.1/4.3-fold accelerated phase-locked single neuron spiking due to 4.0/4.2 mV depolarization while spike jitter decreased to 64/42% of the control, respectively. Raising extracellular K+ from 3 to 9 mM increased the LFP rate 1.4-fold or elicited slower multipeak events. A blockade of Cl−-mediated inhibition with gabazine (5 μM) plus strychnine (10 μM) affected neither the control rhythm nor AMPA/KA oscillations. GYKI-53655 (25 μM) blocked AMPA (but not KA) oscillations whereas UBP-302 (25 μM) blocked KA (but not AMPA) oscillations. Our findings revealed that AMPA and KA evoke a similar novel neural network discharge pattern transformation type by acting on pharmacologically distinct AMPAR and KA receptors. This shows that already the neonatal LC can generate oscillatory network behaviors that may be important, for example, for responses to opioids.
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Dissertations / Theses on the topic "AMPA"

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He, Kaiwen. "AMPA Receptor and synaptic plasticity." College Park, Md.: University of Maryland, 2009. http://hdl.handle.net/1903/9181.

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Thesis (Ph.D.) -- University of Maryland, College Park, 2009.
Thesis research directed by: Dept. of Biology. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.
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Voss, Oliver Paul. "AMPA receptor potentiators : mechanisms of neuroplasticity." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/25276.

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The AMPA receptor potentiator LY404187 is able to significantly increase the average length of neuritic processes in the neuroblastoma cell line SH-SY5Y only in the presence of s-AMPA, and this response is dependent on AMPA receptor activation. The compound also increases neurofilament protein levels as well as levels of the BDNF receptor Trk-B. The increase in neuritic length is blocked by addition of an antibody specific for BDNF indicating that this neurotrophin is required for the induction of neurite growth. The ability to induce morphological change in neuronal processes of the compound was then tested in a rodent model of lesions and sprouting. Unilateral ibotenic lesions of the entorhinal cortex in mice produce a progressive and substantial loss of synapses in the molecular layer of the dentate gyrus. Twice daily s.c. injections of LY404187 for 14 and 28 days post-lesion did not produce any significant change in synaptophysin immunoreactivity in the dentate gyrus. There was also no change in the volume of the lesion in the entorhinal cortex. In a secondary study the rate of neurogenesis in the dentate gyrus was also measured. Administration of LY404187 failed to induce a change in the number of BrdU +ve cells within the sub-granular zone of the dentate gyrus. Any long term structural of behavioural change caused by prolonged AMPA receptor potentiation is likely to be underpinned by changes in protein expression. The levels of key proteins involved in the intracellular response to AMPA receptor activation were measured by Western Blot and immunohistochemistry and levels of the neurotransmitters dopamine and serotonin were measured by HPLC. The effect of chronic administration to the AMPA receptor potentiator LY450108 on the rate of neurogenesis and the development of newly born neuron in the hippocampus was also investigated.
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Man, Hengye. "AMPA receptor trafficking and synaptic plasticity." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ58616.pdf.

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Fowler, Jill H. "AMPA receptors : role in brain injury." Thesis, University of Glasgow, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274788.

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LAMBOLEZ, BERTRAND. "Structure et fonction des recepteurs ampa." Paris 6, 1991. http://www.theses.fr/1991PA066542.

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Le recepteur ampa est un recepteur-canal dont l'agoniste naturel est le neurotransmetteur glutamate. Nous avons etudie le recepteur ampa exprime dans l'ovocyte de xenope a partir de l'adn complementaire d'une de ses sous-unites, glur1 ou a partir d'arn messagers de cerveau de rat. L'etude fonctionnelle de glur1 montre qu'il repond au kainate et a l'ampa et suggere que le recepteur ampa des neurones est un heteromere qui serait responsable des effets electrophysiologiques de l'ampa et du kainate, precedemment attribues a deux recepteurs distincts. Le recepteur ampa est autoinhibe par les agonistes de type ampa: quand on augmente la concentration d'agoniste, la reponse atteint un maximum avant de decroitre. Cette autoinhibition est reservee par des antagonistes competitifs, qui diminuent le taux d'occupation du recepteur par l'agoniste. La diminution de la reponse est interpretee comme une augmentation de la proportion de recepteurs desensibilises. Le recepteur ampa a donc des proprietes pharmacologiques dont l'originalite tient aux particularites de sa desensibilisation. Un modele de la desensibilisation de ce recepteur est propose
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Kuusinen, Arja. "Structure-function relations in AMPA receptors." Helsinki : University of Helsinki, 2000. http://ethesis.helsinki.fi/julkaisut/mat/bioti/vk/kuusinen/.

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Riva, Irene. "Biophysical properties of AMPA receptor complexes." Doctoral thesis, Humboldt-Universität zu Berlin, 2020. http://dx.doi.org/10.18452/21299.

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Die exzitatorische Neurotransmission im gesamten Zentralnervensystem (ZNS) der Wirbeltiere wird weitgehend durch die α-Amino-3-hydroxy-5-methyl-4-isoxazolpropionsäure-Rezeptoren (AMPARs) vermittelt. AMPARs sind Glutamat-gesteuerte Ionenkanäle, die sich an der postsynaptischen Membran befinden, wo sie den Kern makromolekularer Komplexe mit einer Reihe von Hilfsproteinen bilden, die die Rezeptorfunktion konzertiert regulieren. Die bekanntesten dieser Proteine sind die transmembranen AMPA-Rezeptor-Regulierungsproteine (TARPs). TARPs zeigen eine verwirrende Reihe von Effekten auf den Handel, die synaptische Verankerung, die Gate-Kinetik und die Pharmakologie von AMPARs. Über die strukturellen Merkmale des AMPAR-TARP-Komplexes wurde zunehmendes Wissen gesammelt. Die molekularen Mechanismen, die der TARP-Modulation der AMPARs zugrunde liegen, sind jedoch noch nicht vollständig aufgeklärt. In der vorliegenden Studie wurden die AMPAR-TARP-Interaktionen mit Hilfe der Elektrophysiologie in 293 Zellen der menschlichen embryonalen Niere (HEK) untersucht. Die Rolle der extrazellulären TARP-Schleifen, Loop1 (L1) und Loop2 (L2), bei der Modulation der AMPAR-Ansteuerung wurde analysiert. Es wurde ein Modell für die TARP-Modulation vorgeschlagen, das auf vorhergesagten zustandsabhängigen Wechselwirkungen von TARP L1 und L2 mit dem AMPAR basiert. Da die nativen AMPARs im Gehirn hauptsächlich aus heterotetrameren Zusammensetzungen von vier verschiedenen Untereinheiten (GluA1-4) bestehen, wurden außerdem verschiedene Zusammensetzungen von AMPAR-Untereinheiten getestet. Es wurden sowohl gemeinsame als auch von den Untereinheiten abhängige Mechanismen der AMPAR-Modulation durch TARPs beobachtet. Zusammenfassend liefern diese Experimente den Nachweis, dass TARP L1 und L2 nicht an der Assoziation von AMPAR-TARP-Komplexen beteiligt sind und die Modulation der AMPAR-Ansteuerung durch TARPs vollständig erklären können.
Excitatory neurotransmission throughout the vertebrate central nervous system (CNS) is largely mediated by the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs). AMPARs are glutamate-gated ion channels located at the postsynaptic membrane, where they compose the hub of macromolecular complexes with a number of auxiliary proteins that concertedly regulate the receptor function. Among these proteins the most known ones are the transmembrane AMPA receptor regulatory proteins (TARPs). TARPs show a bewildering array of effects on the trafficking, synaptic anchoring, gating kinetics and pharmacology of AMPARs. Growing knowledge has been gathered about the structural features of the AMPAR-TARP complex. However, the molecular mechanisms underlying TARP modulation of AMPARs have not been fully revealed yet. Given that higher brain functions rely upon AMPAR activity and dysregulation of AMPARs has been associated to life-threatening CNS disorders, big efforts are being made to unravel the molecular machinery behind AMPAR regulation and to identify AMPAR auxiliary proteins as potential pharmacological targets. In the present study, AMPAR-TARP interactions were investigated using electrophysiology in human embryonic kidney (HEK) 293 cells. The role of TARP extracellular loops, Loop1 (L1) and Loop2 (L2), in the modulation of AMPAR gating was analysed. A model for TARP modulation has been proposed, based on predicted state-dependent interactions of TARP L1 and L2 with the AMPAR. Moreover, considering that native AMPARs in the brain mainly consist of heterotetrameric assemblies of four distinct subunits (GluA1-4), different AMPAR subunit compositions were tested. Common as well as subunit-dependent mechanisms of AMPAR modulation by TARPs have been observed. In summary, these experiments provided evidence that TARP L1 and L2 are not involved in association of AMPAR-TARP complexes and can entirely account for the modulation of AMPAR gating by TARPs.
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Dev, Kumlesh Kumar. "Regulation of AMPA receptors in rat CNS." Thesis, University of Bristol, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337228.

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Strehlow, Friederike Charlotte [Verfasser], and Nikolaj [Akademischer Betreuer] Klöcker. "Cornichon-Proteine - neue Untereinheiten der AMPA-Rezeptoren." Freiburg : Universität, 2012. http://d-nb.info/1123469946/34.

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Borchardt, Thilo. "Die Konstruktion von Mäusen mit veränderten AMPA-Rezeptoren." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=96489954X.

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Books on the topic "AMPA"

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Cameron, Billie-Rose. Sensitivity of AMPA/Kainate receptors to pentobarbital. Ottawa: National Library of Canada, 1994.

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Tsikritea-Chōreanthē, Helenē. Hē erōmenē tou Ali Ampa: Historiko mythistorēma. Athēna: Ankyra, 2002.

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Rammes, Gerhard. Effects of AMPA receptor modulators on synaptic transmission and long-term potentiation (LTP). Birmingham: University of Birmingham, 1995.

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Manalo, Jerrie Lynn. Interaction between recombinant AMPA receptors and the human immunodeficiency type 1 TAT protein. Ottawa: National Library of Canada, 1998.

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Toong, Samuel Y. Modulation of [alpha]-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptors by a novel organic nitrate ester. Ottawa: National Library of Canada, 1999.

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Park, Eugene. Characterization of changes in ampa receptor subunit expression in spinal cord white matter following acute compression spinal cord injury in the rat. Ottawa: National Library of Canada, 2002.

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Ke, Vēṇukkuṭṭan Nāyar Pi. Amma, Ēlaṃkuḷaṃ Manakkale Amma. Kottayam: Ḍi. Si. Buks, 1999.

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Amba. Poltava: Izd-vo "Poltava", 1997.

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Choodamani, R. Amma. Madras: T. S. Raamalinghoam, 1987.

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Batt, Razia. Amma. Lahore: Mavara pub., 1988.

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Book chapters on the topic "AMPA"

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Scherrmann, Jean-Michel, Kim Wolff, Christine A. Franco, Marc N. Potenza, Tayfun Uzbay, Lisiane Bizarro, David C. S. Roberts, et al. "AMPA Receptor." In Encyclopedia of Psychopharmacology, 77. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1325.

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Tomita, S. "AMPA Receptor." In Handbook of Neurochemistry and Molecular Neurobiology, 345–60. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-30370-3_18.

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Roberts, Patrick D. "AMPA Glutamate Receptor (AMPA Receptor), Conductance Models." In Encyclopedia of Computational Neuroscience, 153–55. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-6675-8_344.

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Roberts, Patrick. "AMPA Glutamate Receptor (AMPA Receptor), Conductance Models." In Encyclopedia of Computational Neuroscience, 1–3. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-7320-6_344-1.

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Morrow, John A., John K. F. Maclean, and Craig Jamieson. "AMPA Receptor Positive Modulators." In Targets and Emerging Therapies for Schizophrenia, 187–231. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2012. http://dx.doi.org/10.1002/9781118309421.ch7.

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Salussolia, Catherine L., Quan Gan, and Lonnie P. Wollmuth. "Assaying AMPA Receptor Oligomerization." In Ionotropic Glutamate Receptor Technologies, 3–14. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-2812-5_1.

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Passafaro, Maria, and Carlo Sala. "AMPA Receptor and Synaptic Plasticity." In Excitotoxicity in Neurological Diseases, 65–77. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-8959-8_5.

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Stöcker, W. "Autoantikörper gegen Glutamat-Rezeptoren Typ AMPA." In Springer Reference Medizin, 284–85. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_382.

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Stöcker, W. "Autoantikörper gegen Glutamat-Rezeptoren Typ AMPA." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_382-1.

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Maul, Corinna, and Bernd Sundermann. "Glutamate Receptors: 7.3 AMPA and Kainate Receptors." In Analgesics, 429–34. Weinheim, FRG: Wiley-VCH Verlag GmbH & Co. KGaA, 2005. http://dx.doi.org/10.1002/3527605614.ch7c.

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Conference papers on the topic "AMPA"

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Peacock, A. W., and M. I. B. Ibrahim. "Infill Oil Development in South West Ampa Field." In SPE Asia Pacific Oil and Gas Conference and Exhibition. Society of Petroleum Engineers, 1997. http://dx.doi.org/10.2118/38063-ms.

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Sorokina, Elena Gennad’evna, Zhanna B. Semenova, Oksana V. Globa, Olga V. Karaseva, Valentin P. Reutov, Galina A. Ignatieva, Sofya A. Afanasieva, et al. "AUTOIMMUNE RESPONSE OF GLUTAMATE RECEPTORS AND NITRIC OXIDE IN EPILEPSY AND TRAUMATIC BRAIN INJURY." In International conference New technologies in medicine, biology, pharmacology and ecology (NT +M&Ec ' 2020). Institute of information technology, 2020. http://dx.doi.org/10.47501/978-5-6044060-0-7.23.

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Abstract:
In children with epilepsy and traumatic brain injury (TBI), the content of autoantibodies (aAb) to glutamate receptors (NMDA and AMPA subtypes) and the level of nitric oxide products - nitrothyrosine (NT) and nitrates/ nitrites (NOx) in the blood were studied. The obtained data make it possible to reveal the specificity of damage to AMPA and NMDA subtypes of glutamate receptors in convulsive states and posttraumatic brain injuries. The participation of NO and its products in the development of autoimmune response was revealed.
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Lau, Hon Chung, Robert Deutman, Salim Al-Sikaiti, and Victor Adimora. "Intelligent Internal Gas Injection Wells Revitalise Mature S.W. Ampa Field." In SPE Asia Pacific Improved Oil Recovery Conference. Society of Petroleum Engineers, 2001. http://dx.doi.org/10.2118/72108-ms.

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Gireli, Giovanna, and Cassiana Raimundo. "Método analítico para determinação de glifosato e AMPA em amostras ambientais." In Congresso de Iniciação Científica UNICAMP. Universidade Estadual de Campinas, 2019. http://dx.doi.org/10.20396/revpibic2720192410.

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Li, Nanyu, and Charles C. Zhou. "AMPA-Net: Optimization-Inspired Attention Neural Network for Deep Compressed Sensing." In 2020 IEEE 20th International Conference on Communication Technology (ICCT). IEEE, 2020. http://dx.doi.org/10.1109/icct50939.2020.9295956.

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Kairat, Bakhytzhan, Sergei Gaidin, Valery Zinchenko, Sergei Mayorov, Denis Laryushkin, and Artem Kosenkov. "A METHOD OF VITAL IDENTIFICATION OF NEURONS CONTAINING CALCIUM-PERMEABLE AMPA RECEPTORS." In XVIII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2022. http://dx.doi.org/10.29003/m2776.sudak.ns2022-18/154-155.

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Amaro Gireli, Giovanna, and CASSIANA CAROLINA MONTAGNER RAIMUNDO. "Método analítico para a determinação de glifosato e AMPA em amostras ambientais." In XXV Congresso de Iniciação Cientifica da Unicamp. Campinas - SP, Brazil: Galoa, 2017. http://dx.doi.org/10.19146/pibic-2017-77933.

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Hosokawa, Chie, Tatsunori Kishimoto, Yasuyo Maezawa, Suguru N. Kudoh, and Takahisa Taguchi. "Optical trapping of quantum-dot conjugated AMPA-type receptors depend on initial assembling states." In Optical Manipulation and Structured Materials Conference, edited by Takashige Omatsu, Hajime Ishihara, and Keiji Sasaki. SPIE, 2018. http://dx.doi.org/10.1117/12.2319362.

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Salleh, Mohamad Seruddin, and Sagar Ronghe. "Reservoir characterization on thin sands in South West Ampa 21 area (BLK11) using seismic inversion." In SEG Technical Program Expanded Abstracts 1999. Society of Exploration Geophysicists, 1999. http://dx.doi.org/10.1190/1.1820823.

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Ferreira, Giovanna, Nadia Rodrigues, and Ana Souza. "Resíduos de Glifosato e AMPA em fórmula infantil à base de soja: monitoramento do mercado brasileiro." In Congresso de Iniciação Científica UNICAMP. Universidade Estadual de Campinas, 2019. http://dx.doi.org/10.20396/revpibic2720192608.

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Reports on the topic "AMPA"

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Wiarda, Dorothea, Goran Arbanas, Andrew Holcomb, and Marco Pigni. NCSP Analytical Methods Subtask 3 & NCSP Nuclear Data Subtask 6: AMPX Development and Maintenance & SAMMY Modernization. Office of Scientific and Technical Information (OSTI), September 2019. http://dx.doi.org/10.2172/1907404.

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Wiarda, Dorothea, Goran Arbanas, Andrew Holcomb, and Marco Pigni. NCSP Analytical Methods Subtask 3 & NCSP Nuclear Data Subtask 6: AMPX Development and Maintenance & SAMMY Modernization. Office of Scientific and Technical Information (OSTI), September 2019. http://dx.doi.org/10.2172/1922330.

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Dawson, Bruce, David S. Day, and Alice Mulvehill. The AMPS. Fort Belvoir, VA: Defense Technical Information Center, July 1990. http://dx.doi.org/10.21236/ada225988.

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HONEYMAN, J. O. MERCURY & DIMETHYLMERCURY EXPOSURE & EFFECTS. Office of Scientific and Technical Information (OSTI), December 2005. http://dx.doi.org/10.2172/861943.

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Harris, J. M., and P. J. McDaniel. AIM: An AMPX module. Office of Scientific and Technical Information (OSTI), September 1988. http://dx.doi.org/10.2172/6721784.

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Mondragon, Krystal L. AMPP Newsletter - Feb 2020. Office of Scientific and Technical Information (OSTI), February 2020. http://dx.doi.org/10.2172/1601615.

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Mondragon, Krystal L. AMPP Newsletter - May 2020. Office of Scientific and Technical Information (OSTI), May 2020. http://dx.doi.org/10.2172/1623422.

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Mondragon, Krystal L. AMPP Newsletter - November 2019. Office of Scientific and Technical Information (OSTI), November 2019. http://dx.doi.org/10.2172/1573981.

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Mondragon, Krystal. AMPP Newsletter - Sep 2020. Office of Scientific and Technical Information (OSTI), September 2020. http://dx.doi.org/10.2172/1663175.

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Mondragon, Krystal. AMPP Newsletter - Feb 2021. Office of Scientific and Technical Information (OSTI), March 2021. http://dx.doi.org/10.2172/1771087.

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