ampa glutamate receptor

Der Strom durch Rezeptoren ohne GluR2 ist einwrts rektifizierend. 182186, 1997. showed that relatively high external calcium (1mM) potentiates GABA-b receptors via CaSR, while relatively low calcium (0.01mM) inhibits them (Wise etal., 1999). [16], Memantine is an example of an uncompetitive channel blocker of the NMDA receptor, with a relatively rapid off-rate and low affinity. [26] Before this finding, memantine, another adamantane derivative, had been synthesized by Eli Lilly and Company in 1963. (EAE) and the implications for multiple sclerosis treatment, Multiple Sclerosis, vol. subtypes of glutamate receptor, Neuron, vol. C Bolton, D Parker, J McLeod, and J L Turk, A study of the prostaglandin and thromboxane content of the central nervous tissues with the development of chronic Severe side effects may include blood clots, psychosis, and heart failure. [20] AMPARs open and close quickly (1ms), and are thus responsible for most of the fast excitatory synaptic transmission in the central nervous system. [118][119][120][121][122] Tianeptine also acts on the NMDA and AMPA receptors. 80, no. 1, pp. For the submarine, see, Second generation derivative of memantine; nitromemantine, Maher, T.J. (2013). 11, pp. Transmembrane AMPA receptor regulatory proteins (TARPs) are a family proteins that associate with AMPA receptors and control their trafficking and conductance. When certain NMDA receptor antagonists are given to rodents in large doses, they can cause a form of brain damage called Olney's lesions. This model nicely explains the upshift of the resting membrane potential toward the firing threshold when the external calcium is low. As such, it was described as nonsynaptic epileptiform activity, suggesting a change of intrinsic properties of individual neurons independent of network activity. [42] Myosin proteins are calcium sensitive motor proteins that have also been found to be essential for AMPA receptor trafficking. For the most part, the resting membrane potential is determined by the potassium gradient across the cell membrane. 17, no. NICE technology appraisal January 18, 2011. NMDAR-targeted compounds, including ketamine, esketamine (JNJ-54135419), rapastinel (GLYX-13), apimostinel (NRX-1074), zelquistinel (AGN-241751), 4-chlorokynurenine (AV-101), and rislenemdaz (CERC-301, MK-0657), are under development for the treatment of mood disorders, including major depressive disorder and treatment-resistant depression. [47] One study suggests that reelin may play a role in the NMDA receptor maturation by increasing the GluN2B subunit mobility. More importantly, each GluN2 subunit has a different intracellular C-terminal domain that can interact with different sets of signalling molecules. The NMDA receptor is a glutamate and ion channel protein receptor that is activated when glycine and glutamate bind to it. Extrasynaptic NMDA receptors promote death signaling; they cause transcriptional shut-off, mitochondrial dysfunction, and structural disintegration. 3, pp. 3, pp. Compared to dopaminergic stimulants like methamphetamine, the NMDAR antagonist phencyclidine can produce a wider range of symptoms that resemble schizophrenia in healthy volunteers, in what has led to the glutamate hypothesis of schizophrenia. 2131, 1995. Alpha-amino-3-dyroxy-5-methyl-4-isoxazolepropionic acid (AMPA) Receptor Channel. 53, no. YM90K showed potent suppressive activity against audiogenic seizure in DBA/2 mice; ED50 values of YM90K and NBQX against tonic seizure were 2.54 and 7.17 mg/kg (i.p. Native responses of the GABA C receptor type occur in retinal bipolar or horizontal cells across vertebrate species.. GABA receptors are exclusively composed of (rho) subunits that are NMDA Receptor Function. NALCN=Na+ leaky channel; voltage-gated sodium channel=voltage-gated sodium channel; KCa=calcium-activated potassium channel; CNG=cyclic nucleotide-gated ion channels; EPSC=excitatory postsynaptic current; CaSR=calcium sensing receptors. 136, no. RC185.1RC185.6, 2001. Magnesium works to potentiate NMDA-induced responses at positive membrane potentials while blocking the NMDA channel. J W Olney, Brain lesions, obesity, and other disturbances in mice treated with monosodium glutamate, Science, vol. proposed a model linking external calcium and the NALCN via the CaSR, activation of G-protein, and the UNC80/UNC79 protein complex (Lu etal., 2010). The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article. The authors receive no financial support for the research; the authorship and the article publication was supported by Barrow Neurological Foundation. 493503, 1997. This allows the transcription factors in the nucleus to respond differently based in the phosphorylation state of Jacob. Measuring serum calcium in dialysis patients, Mutneja M., Berton F., Suen K. F., Luscher C., Slesinger P. A. 3, pp. The mechanism for LTP has long been a topic of debate, but, recently, mechanisms have come to some consensus. Several types of ionotropic glutamate receptors have been identified. GABA-a receptors are the molecular base for inhibitory postsynaptic current. Memantine (1-amino-3,5-dimethyladamantane) is an aminoalkyl cyclohexane derivative and an atypical drug compound with non-planar, three dimensional tricyclic structure. It is taken by mouth. PMC legacy view 1, pp. 2, pp. H Koenig, A D Goldstone, and C Y Lu, Blood-brain barrier breakdown in cold-injured brain is linked to a biphasic stimulation of ornithine decarboxylase activity and polyamine 2011; Santangelo et al. P Klivenyi, K Kekesi, G Juhasz, and L Vecsei, Amino acid concentrations in cerebrospinal fluid of patients with multiple sclerosis, Acta Neurologica Scandinavica, vol. Theanine provides a unique brothy or B. im Hippokampus oder im Kleinhirn, wird die Dichte der AMPA-Rezeptoren in der postsynaptischen Membran abhngig von der Aktivitt der Synapse reguliert. Es resultiert in 38 Aminosureresten, die der letzten Transmembrandomne vorangestellt sind. 553555, 2004 (German). [31] Blocking either this influx or the activation of CaMKII prevents LTP, showing that these are necessary mechanisms for LTP. In the opposing postsynaptic cell, glutamate receptors, such as the NMDA receptor or the AMPA receptor, bind glutamate and are activated. NMDA receptor antagonists that have been shown to induce Olney's lesions include ketamine, phencyclidine, and dextrorphan (a metabolite of dextromethorphan), as well as some NMDA receptor antagonists used only in research environments. Because the glutamate receptor proteins are expressed on the surface of the cells in such a way that they can only be activated from the outside, it follows that glutamate exerts its neurotransmitter function from the extracellular fluid. Almost all of the GluA2 subunits in CNS are edited to the GluA2(R) form. YM90K co-injected with AMPA or kainate into the rat striatum protected cholinergic neurons against AMPA- or kainate-induced neurotoxicity. 12491254, 1997. [19], There are eight variants of the GluN1 subunit produced by alternative splicing of GRIN1:[33], While a single GluN2 subunit is found in invertebrate organisms, four distinct isoforms of the GluN2 subunit are expressed in vertebrates and are referred to with the nomenclature GluN2A through GluN2D (encoded by GRIN2A, GRIN2B, GRIN2C, GRIN2D). [32], The GluN2B subunit has been involved in modulating activity such as learning, memory, processing and feeding behaviors, as well as being implicated in number of human derangements. Thomas JM, Levy RB, Mahadomrongkul V, Shirao T, Aoki C, Huerta PT. [14][15][16][17] Blocking of NMDA receptors could therefore, in theory, be useful in treating such diseases. G S Plaut, Effectiveness of amantadine in reducing relapses in multiple sclerosis, Journal of the Royal Society of Medicine, vol. However the affinity could not be too low and dwell time not too short (as seen with Mg2+) where membrane depolarization relieves the block. 14151419, 1992. neuronal dysfunction, Brain: A Journal of Neurology, vol. 11, no. An vielen Synapsen, wie z. 6638, pp. Succinic semialdehyde dehydrogenase deficiency (SSADHD) is a rare autosomal recessive disorder of the degradation pathway of the inhibitory neurotransmitter -aminobutyric acid, or Full activation of NMDA receptors is both voltage-gated and ligand-gated. encephalomyelitis, Journal of Neurochemistry, vol. The external calcium modulation of GABA-b would be established only if the experimental calcium concentration could have been extrapolated to the range of 1 to 3mM. The activity of NMDA receptors is also strikingly sensitive to the changes in, NMDA receptor function is also strongly regulated by chemical reduction and oxidation, via the so-called "redox modulatory site. E M Flanagan, J B Erickson, O H Viveros, S Y Chang, and J F Jr Reinhard, Neurotoxin quinolinic acid is selectively elevated in spinal cords of rats with experimental allergic [35] Unlike GluN1 subunits, GluN2 subunits are expressed differentially across various cell types and developmental timepoints and control the electrophysiological properties of the NMDA receptor. The Journal of Physiology publishes original research in all areas of physiology and pathophysiology that illustrates new physiological principles or mechanisms. 9, pp. 9, pp. [54] Treatment for these conditions might be found in blocking NMDA receptors not found at the synapse. Subunit compositions are determined at the time of modification at the rough ER. Besides AHP, firing frequency is also determined by injected positive DC. There is no direct examination of the effects of external calcium on GABA-Cl current. 3740, 1996. For example, adding positive-charged calcium ions to a 70mV transmembrane potential may perhaps bring the apparent electric field down to 80mV, therefore making the ion channels located across the cell membrane feel like they are in an ambient electric field of 80mV. The condition predominantly affects young adults and is characterised by immunological and inflammatory changes in the periphery and CNS that contribute to neurovascular disruption, haemopoietic cell invasion of target tissues, and demyelination of H-G Bernstein and M Mller, The cellular localization of the L-ornithine decarboxylase/polyamine system in normal and Glutamate receptors are one of four categories, three of which are ligand-gated ion channels and one of which is a G-protein coupled receptor (often referred to as GPCR). Ein negativer allosterischer Modulator ist Ethanol. H Parfenova, A Fedinec, and C W Leffler, Ionotropic glutamate receptors in cerebral microvascular endothelium are functionally linked to heme This means that the principal ions gated by AMPARs are sodium and potassium, distinguishing AMPARs from NMDA receptors (the other main ionotropic glutamate receptors in the brain), which also permit calcium influx. 5057, 2002. Alpha-amino-3-dyroxy-5-methyl-4-isoxazolepropionic acid (AMPA) Receptor Channel. The presence of a GluA2 subunit will almost always render the channel impermeable to calcium. [73] 1-2, p. 188, 1994. Glutamate exerts its effects by binding to and activating cell surface receptors.In mammals, four families of glutamate receptors have been identified, known as AMPA receptors, kainate receptors, NMDA receptors, and metabotropic glutamate receptors.The first three families are ionotropic, meaning that when activated they open membrane channels that allow ions to pass Bundling up excitement, Nature, vol. The methyl side groups play an important role in increasing the affinity to the open NMDA receptor channels and making it a much better neuroprotective drug than amantadine. [126] Experiments in which rodents are treated with NMDA receptor antagonist are today the most common model when it comes to testing of novel schizophrenia therapies or exploring the exact mechanism of drugs already approved for treatment of schizophrenia. 357371, 1994. government site. It is taken by mouth. -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, better known as AMPA, is a compound that is a specific agonist for the AMPA receptor, where it mimics the effects of the neurotransmitter glutamate.[1]. The simplest explanation for LTP is as follows (see the long-term potentiation article for a much more detailed account). [12][13][14], Overactivation of the receptor, causing excessive influx of Ca2+ can lead to excitotoxicity which is implied to be involved in some neurodegenerative disorders. M Nishi, H Hinds, H-P Lu, M Kawata, and Y Hayashi, Motoneuron-specific expression of NR3B, a novel NMDA-type glutamate receptor subunit that works The NMDA receptor is an ionotropic receptor that allows for the transfer of electrical signals between neurons in the brain and in the spinal column. 719721, 1969. Divalent ions contribute less current but have higher affinity to the pore due to their relatively heavier positive charges. This property of the NMDA receptor explains many aspects of long-term potentiation (LTP) and synaptic plasticity.[113]. J W Prineas, R O Barnard, E E Kwon, L R Sharer, and E-S Cho, Multiple sclerosis: remyelination of nascent lesions, Annals of Neurology, vol. 255266, 1990. The NMDA receptor forms a heterotetramer between two GluN1 and two GluN2 subunits (the subunits were previously denoted as GluN1 and GluN2), two obligatory GluN1 subunits and two regionally localized GluN2 subunits. 6, pp. Excitotoxicity refers to the pathological process by which neurons are damaged and killed by the overactivations of receptors, such as [51] A theta burst stimulation that usually induces LTP with synaptic NMDARs, when applied selectively to extrasynaptic NMDARs produces a LTD.[61] Experimentation also indicates that extrasynaptic activity is not required for the formation of LTP. Agonists NMDA receptors need both glutamate and glycine to bind to the receptor in order to produce a biological effect. 23, no. The -NH2 group on memantine, which is protonated under physiological pH of the body, represents the region that binds at or near to the Mg2+ site. [8] When the four subunits of the tetramer come together, this second membranous domain forms the ion-permeable pore of the receptor. 52, no. Glutamate is the primary excitatory neurotransmitter in the central nervous system and opens non-selective cation channels. AMPA-Rezeptoren sind wichtig fr die synaptische Plastizitt. 141142, 2000. F P Monnet, G Debonnel, and C de Montigny, The cytochromes P-450 are not involved in the modulation of the N-methyl-D-aspartate response by sigma ligands in 387407, 2003. These glutamate receptors are named after the agonists that activate them: NMDA (N-methyl-D-aspartate), AMPA (-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate), and kainic These findings demonstrate a novel effect for resveratrol on glutamate receptor regulation, a process that may underlie the cognitive benefits of resveratrol on brain function. 1, pp. We keep in mind readers who may have less background on ion channel physiology. The first case was identified in 1981 and published in a Dutch The main problem with the utilization of NMDA receptor antagonists for neuroprotection is that the physiological actions of the NMDA receptor are essential for normal neuronal function. NOTE: You selected the 'Send Payment' option for your registration. Summation, which includes both spatial summation and temporal summation, is the process that determines whether or not an action potential will be generated by the combined effects of 12, no. B A t Hart and S Amor, The use of animal models to investigate the pathogenesis of neuroinflammatory disorders of the central [27] There is one GluN1, four GluN2, and two GluN3 subunit encoding genes, and each gene may produce more than one splice variant. 12, pp. Memantine binds at or near to the Mg2+ site inside the NMDA receptor associated channel. The NMDA receptor is one of three types of ionotropic glutamate receptors, the other two being AMPA and kainate receptors. C Bolton, A M Turner, and J L Turk, Prostaglandin levels in cerebrospinal fluid from multiple sclerosis patients in remission and relapse, Journal of Neuroimmunology, vol. YM90K co-injected with AMPA or kainate into the rat striatum protected cholinergic neurons against AMPA- or kainate-induced neurotoxicity. [43] For instance, greater ratios of the GluN2B subunit leads to NMDA receptors which remain open longer compared to those with more GluN2A. Theanine / i n i n /, also known as L--glutamylethylamide and N 5-ethyl-L-glutamine, is an amino acid analogue of the proteinogenic amino acids L-glutamate and L-glutamine and is found primarily in particular plant and fungal species.It was discovered as a constituent of green tea in 1949; in 1950, it was isolated from gyokuro leaves. FOIA In Anwesenheit von GluR2 ist die Strom-Spannungs-Beziehung von AMPA-Rezeptoren dagegen linear. 1-2, pp. Therefore, these channels need to overcome a larger hurdle to activate. S R Bowman, G S Scott, and C Bolton, Glutamate stimulates peroxynitrite production in a brain-derived endothelial cell line via While the amino acid sequence of the subunit indicated that there seemed to be four transmembrane domains (parts of the protein that pass through the plasma membrane), proteins interacting with the subunit indicated that the N-terminus seemed to be extracellular, while the C-terminus seemed to be intracellular. Because the Kir is only weakly inhibited by external calcium (Wegner, 1994), the contribution of Kir modulation in the situation of low external calcium may be small, if any. 125, no. 90, no. Die Polypeptidkette einer Untereinheit durchquert die Membran drei Mal und bildet in der Membran von der intrazellulren Seite her eine Schleife. Work by Dreixler and Leonard attempted to highlight the role of calcium, along with another ionzincin AMPA current potentiation. It is the valleys depth (AHP amplitude) that determines the time interval before reaching back to the next firing threshold. [51][52][53] Because NMDA receptors play an important role in the health and function of neurons, there has been much discussion on how these receptors can affect both cell survival and cell death. A40A47, 1999. [74], Other partial agonists of the NMDA receptor acting on novel sites such as rapastinel (GLYX-13) and apimostinel (NRX-1074) are now viewed for the development of new drugs with antidepressant and analgesic effects without obvious psychotomimetic activities. 4, no. 11921196, 1995. Changes in H+ concentration can partially inhibit the activity of NMDA receptors in different physiological conditions. 2, pp. [93] The https:// ensures that you are connecting to the Die einzelnen Untereinheiten bestehen aus rund 900 Aminosuren. GluN1-1a, GluN1-1b; GluN1-1a is the most abundantly expressed form. Unlike many other NO donors, alkyl nitrates do not have potential NO associated neurotoxic effects. However, the NMDA receptor cation channel is blocked by Mg2+ at resting membrane potential. The GluA1 and GluA4 subunits consist of a long carboxy (C)-tail, whereas the GluA2 and GluA3 subunits consist of a short carboxy-tail. [78][79][115] In addition, ketamine is already employed for this purpose as an off-label therapy in some clinics.[116][117]. 2, pp. 145161, 2003. 1, pp. 179182, 1992. antagonists, Journal of Neural Transmission, vol. The numerical definition of high or low calcium was not uniform among these studies. Wise etal. They are also known as "CX compounds". The Ca2+ can in turn function as a second messenger in various signaling pathways. If an AMPAR lacks GluA2 subunits, then it is susceptible to being blocked in a voltage-dependent manner by a class of molecules called polyamines. HHS Vulnerability Disclosure, Help induced rotations in substantia nigra lesioned rats, Neuroscience Letters, vol. [47][48] This pathway is responsible for the maintenance of new memories, sustaining the transient changes resulting from the regulated pathway. The receptor was first named the "quisqualate receptor" by Watkins and colleagues after a naturally occurring agonist quisqualate and was only later given the label "AMPA receptor" after the selective agonist developed by Tage Honore and colleagues at the Royal Danish School of Pharmacy in Copenhagen. Once payment is received, your registration will be completed and a registration confirmation e-mail will be sent. AMPA-Rezeptoren (AMPAR, englisch -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor) bilden neben den NMDA-und Kainat-Rezeptoren eine Untergruppe der Glutamat-Rezeptoren und sind die verbreitetsten Neurotransmitter-Rezeptoren im Zentralnervensystem.Sie bilden Kationenkanle, welche die schnelle Komponente des postsynaptischen Stroms Hille discovered that high calcium shifted the voltage-dependency of sodium channel activation gates to the right, suggesting that a higher depolarization is necessary to open NaV (Hille, 1968). Depending on its subunit composition, its ligands are glutamate and glycine (or D-serine). This has revealed a common fold with amino acid-binding bacterial proteins and with the glutamate-binding module of AMPA-receptors and kainate-receptors. 2, pp. The binding site with the highest affinity is called the dominant binding site. One possibility is that, during LTP, there is lateral movement of AMPA receptors from perisynaptic sites directly to the PSD. Memantine and newer derivatives could become very important weapons in the fight against neuronal damage. [19] Once open, the channel may undergo rapid desensitization, stopping the current. The use of receptor antagonists to control EAE is also discussed together with the possibility of therapeutic application in demyelinating disease. Anwesenheit eines alternativ gespleiten Exons. 3, pp. [14], Uncompetitive NMDA receptor antagonists block within the ion channel at the Mg2+ site (pore region) and prevent excessive influx of Ca2+. 54, no. Theanine / i n i n /, also known as L--glutamylethylamide and N 5-ethyl-L-glutamine, is an amino acid analogue of the proteinogenic amino acids L-glutamate and L-glutamine and is Thomas Glutamate receptors are synaptic and non synaptic receptors located primarily on the membranes of neuronal and glial cells. The mechanism of desensitization is believed to be due to a small change in angle of one of the parts of the binding site, closing the pore. [3][4][5] Most AMPARs are heterotetrameric, consisting of symmetric 'dimer of dimers' of GluA2 and either GluA1, GluA3 or GluA4. 1-2, p. 86, 2004. The ion channels will only open if the post-synaptic membrane has already been depolarized, and the neurotransmitters glutamate and glycine are attached. 149, no. [38] Another possibility is that exocytosis of intracellular vesicles is responsible for AMPA trafficking to the PSD directly. [21], The subunit composition of the AMPAR is also important for the way this receptor is modulated. This knowledge provides a unifying explanation for the role of hypocalcemic hyperexcitability in seizure activity. 143149, 1995. Ampakines, also stylized as AMPAkines, are a subgroup of AMPA receptor positive allosteric modulators with a benzamide or closely related chemical structure. 75, no. CAMKII enzyme is eventually responsible for the development of the actin cytoskeleton of neuronal cells and, eventually, for the dendrite and axon development (synaptic plasticity). C Matute, E Alberdi, M Domercq, F Prez-Cerd, A Prez-Samartn, and M V Snchez-Gmez, The link between excitotoxic oligodendroglial death and demyelinating diseases, Trends in Neurosciences, vol. NMDA receptor (NMDAR)-mediated currents are directly related to membrane depolarization. The range of external calcium reported in these studies varies from 0 to 5mM. There are three subtypes of glutamate receptors. This observation suggests that external calcium may compete with zinc binding sites on AMPA receptors, and thus high calcium concentrations may inhibit zinc potentiation of AMPA current, whereas low or zero calcium leaves greater freedom for zinc to bind and enhance the AMPA current. (2012), Surface charge impact in low-magnesium model of seizure in rat hippocampus, Kidwell K. S., Kopp W. E., Albano E. A., Brown A. E. (2013), Ghosts in My Body: Seizure-like presentation of hypocalcemic tetany secondary to hypomagnesemia in a patient receiving cetuximab therapy for metastatic medulloblastoma, Kinoshita H., Kokudo T., Ide T., Kondo Y., Mori T., Homma Y., Yakushiji F. (2010), A patient with DiGeorge syndrome with spina bifida and sacral myelomeningocele, who developed both hypocalcemia-induced seizure and epilepsy, Persistence of the olfactory receptor current in a wide variety of extracellular environments, Korkmaz H. A., Dizdarer C., Ecevit C. O. According to this model, high calcium activates the CaSR, which tonically inhibits the NALCN. 12, pp. 13, 1994. (2014), Hypocalcemic seizure in an adolescent with Down syndrome: A manifestation of unrecognized celiac disease, Cyclic nucleotide-gated channels contribute to the cholinergic plateau potential in hippocampal CA1 pyramidal neurons, Lazarevic V., Pothula S., Andres-Alonso M., Fejtova A. [51], Two specific proteins have been identified as a major pathway responsible for these different cellular responses ERK1/2, and Jacob. Thus, higher calcium enhances IA amplitude and removes IA inactivation, which may contribute to a transient shunting of current, leading to a higher firing threshold. 257, no. 64, no. [64] Once the clathrin coat detaches, other proteins can interact directly with the AMPARs using PDZ carboxyl tail domains; for example, glutamate receptor-interacting protein 1 (GRIP1) has been implicated in intracellular sequestration of AMPARs. Neramexane went to clinical trials for four indications, including Alzheimer's disease.[26]. Multiple sclerosis (MS) is a chronic demyelinating disease of the human central nervous system (CNS). determinants of co-agonist potentiation in the extracellular M3-M4 loop region, Proceedings of the National Academy of Sciences of the United States of America, vol. in a dominant-negative manner, The Journal of Neuroscience, vol. [58][59][60], Long-term depression enacts mechanisms to decrease AMPA receptor density in selected dendritic spines, dependent on clathrin and calcineurin and distinct from that of constitutive AMPAR trafficking. Interactions from calcineurin activate dynamin GTPase activity, allowing the clathrin pit to excise itself from the cell membrane and become a cytoplasmic vesicle. 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