The glutamate transporter GLT-1 is crucial for the maintenance of low interstitial glutamate concentrations. by disrupting the association between Hsp90 and GLT-1. Utilizing a style of TLE, we showed that long-term systemic administration of 17AAG significantly suppressed spontaneous repeated seizures and ameliorated astrogliosis. General, these results claim that up-regulation of GLT-1 by inhibiting Hsp90 in reactive astrocytes could be a potential healing focus on for the treating epilepsy and excitotoxicity. Launch Epilepsy is among the most common chronic neurological illnesses, yet around one-third of affected sufferers do not react to anticonvulsive medications PFI-3 supplier that focus on neurons (Kwan et al., 2011). Latest studies claim that astrocytes certainly are a potential focus on for the healing treatment of intractable epilepsy (Hja, 2014; Robel et al., 2015). GLT-1 (EAAT2; slc1a2) is normally predominantly portrayed in astrocytes and in charge of maintaining low extracellular ...
SLC1A1, also known as excitatory amino-acid transporter 3 (EAAT3), is a protein that in humans is encoded by the SLC1A1 gene. Excitatory amino-acid transporter 3 is a member of the high-affinity glutamate transporters which plays an essential role in transporting glutamate across plasma membranes in neurons. In the brain, excitatory amino acid transporters are crucial in terminating the postsynaptic action of the neurotransmitter glutamate, and in maintaining extracellular glutamate concentrations below neurotoxic levels. EAAT3 also transports aspartate, and mutations in this gene are thought to cause dicarboxylic aminoaciduria, also known as glutamate-aspartate transport defect. EAAT3 is also the major route of neuronal cysteine uptake. Cysteine is a component of the major antioxidant glutathione, and mice lacking EAAT3 exhibit reduced levels of glutathione in neurons, increased oxidative stress, and age-dependent loss of neurons, especially neurons of the substantia nigra. SLC1A1 has been ...
In the brain, termination of glutamatergic neurotransmission is achieved predominantly by rapid uptake of synaptically released glutamate into astrocytes through the sodium-dependent glutamate transporters GLT-1 and GLAST and its subsequent conversion to glutamine by the enzyme GS (Rothstein et al., 1996; Sonnewald et al., 1997). To date, several factors, including glutamate itself, have been identified that rapidly alter the activity of the glutamate uptake process by post-translational modification of glutamate transporters (for review, see Gegelashvili and Schousboe, 1998). However, the factor or factors regulating the expression of glial glutamate transporter as well as of GS are still unknown. Pronounced increases in glial expression levels of GLT-1, GLAST, and GS have been observed in coculture systems with neurons (Hayashi et al., 1988; Swanson et al., 1997; Schlag et al., 1998). Although originally it had been suggested that these effects involve glutamate signaling, recent work by ...
Shop Glutamate/aspartate import solute-binding protein ELISA Kit, Recombinant Protein and Glutamate/aspartate import solute-binding protein Antibody at MyBioSource. Custom ELISA Kit, Recombinant Protein and Antibody are available.
In mammalian cells, the uptake of amino acids is mediated by specialized, energy-dependent and passive transporters with overlapping substrate specificities. Most energy-dependent transporters are coupled either to the cotransport of Na+ or Cl- or to the countertransport of K+. Passive transporters are either facilitated transporters or channels. As a prelude to the molecular characterization of the different classes of transporters, we have isolated transporter cDNAs by expression-cloning with Xenopus laevis oocytes and we have characterized the cloned transporters functionally by uptake studies into oocytes using radiolabelled substrates and by electrophysiology to determine substrate-evoked currents. Mammalian transporters investigated include the dibasic and neutral amino acid transport protein D2/NBAT (system b0+) and the Na(+)- and K(+)-dependent neuronal and epithelial high-affinity glutamate transporter EAAC1 (system XAG-). A detailed characterization of these proteins has provided new ...
Najimi, Mustapha ; Stéphenne, Xavier ; Sempoux, Christine ; Sokal, Etienne ; Khuu, Ngoc Dung. Modulation of EAAT-2 glutamate transporter expression in human liver cholestasis.21st Biennial Meeting of the International-Society-for-Neurochemistry/38th Annual Meeting of the American-Society-for-Neurochemistry (Cancun (Mexico), Aug 19-24, 2007). In: Journal of Neurochemistry, Vol. 102, p. 46-47 (2007 ...
There are 30,000 cases of ALS at any given time in the United States. Presently there is no cure for ALS and few treatment options. 90 percent of cases have unk...
We cloned and expressed a human metabotropic glutamate receptor 1 alpha (HmGluR1 alpha) in a novel cell line. The human mGluR1 alpha cDNA was found to be 86% identical to rat mGluR1 alpha, and the predicted protein sequence was found to be 93% identical to rat mGluR1 alpha. We expressed HmGluR1 alpha in AV12-664, an adenovirus-transformed Syrian hamster cell line. To prevent tonic activation of HmGluR1 alpha by glutamate that may be released by these cells into the extracellular medium, HmGluR1 alpha was co-expressed in AV12-664 cells with a rat glutamate/aspartate transporter (GLAST). This allowed investigation of the effect that clearance of glutamate from the extracellular space would have on HmGluR1 alpha function. A comparison of mRNA levels revealed that HmGluR1 alpha was similarly expressed in cells with or without co-expression of GLAST. However, HmGluR1 alpha-mediated phosphoinositide hydrolysis was efficiently elicited only in cells co-expressing rat GLAST. Blockade of glutamate ...
Selected Publications:. Akyuz, N., Georgieva, E. R., Zhou, Z., Stolzenberg, S., Cuendet, M. A.,. Khelashvili, G., Altman,. R. B., Terry, D. S., Freed, J. H., Weinstein, H., Boudker, O.,. Blanchard, S. C.: Transport domain. motions in a glutamate transporter homologue determine turnover rate.. Nature (2015).. ###. Stolzenberg, S., Khelashvili, G., Weinstein, H.: Structural. Intermediates in a Model of the. Substrate Translocation Path of the Bacterial Glutamate Transporter. Homologue GltPh.. J Phys Chem B, 116, 5372-5383 (2012).. ###. Zhao, C.*, Stolzenberg, S.*, Gracia, L., Weinstein, H., Noskov, S., Shi,. L.: Ion-Controlled. Conformational Dynamics in the Outward-Open Transition from an Occluded. State of LeuT.. Biophys J., 103, 878-888 (2012).. * denotes equal contribution ...
Gap detection or gap pre-pulse inhibition of the acoustic startle (GPIAS) has been successfully used in rat and guinea pig models of tinnitus, yet this system has proven to have low efficacy in CBA mice, with low basal GPIAS and subtle tinnitus like effects. Here, we tested five mouse strains (CBA, BalbC, CD-1, C57BL/6 and sv129) for pre-pulse inhibition and gap detection with varying interstimulus intervals (ISI) and found the that mice from a CBA genetic background had the poorest capacities of suppressing the startle response in presence of a pre-pulse or a gap. CD-1 mice displayed variable responses throughout all ISI. Interestingly, C57BL/6, sv129 and BalbC showed efficient suppression with either pre-pulses or gaps with shorter ISI. The glutamate aspartate transporter (GLAST) is expressed in support cells from the cochlea and buffers the excess of glutamate. We hypothesized that loss of GLAST function could sensitize the ear to tinnitus-inducing agents, such as salicylate. Using shorter ISI to
Data from our laboratory have demonstrated that antiexcitotoxic actions are involved in the neuroprotective actions of citicoline.7 Indeed, we found that citicoline is able to reduce infarct volume in parallel to a decrease in ischemia-induced elevation in brain glutamate levels measured by microdialysis. High extracellular glutamate concentrations in the brain may result from increased release and/or from decreased uptake. Ischemia-induced glutamate release has been shown to be largely due to reversed operation of neuronal glutamate transporters, a fact that results from a severe depletion in adenosine 5′-triphosphate levels caused by ischemia.8 Of note, our results also showed that ischemia-induced adenosine 5′-triphosphate loss was decreased both in vivo and in vitro by previous administration of citicoline. These results support the hypothesis that citicoline-induced effect on neuronal adenosine 5′-triphosphate levels accounts, at least in part, for the decrease in extracellular ...
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AJNR 181171 Lloyd GA (1982) Primary orbital meningioma a review of 41 patients investigated radiologically. Protein Kinases and Phosphatases Protein apo naproxen vs naproxen are potent endogenous regulators of glutamate transporter activity, with protein kinase C (PKC), protein kinase A (PKA), and phosphatidylinositol 3-kinase (PI3K) naprxoen implicated in the intracellular control of EAAT activity, expression and cell- surface trafficking.
Table of Contents -- CHAPTER 1: Introduction and Background -- 1.1. Glutamate and the CNS............................................................................................................................................................................................................2-6 -- 1.1.A. Glutamatergic Neurotransmission.............................................................................................................................................................................2 -- 1.1.B. CNS Sources of Glutamate..............................................................................................................................................................................3 -- 1.1.C. Regulation of Extracellular Glutamate Concentrations.................................................................................................................................................3-6 -- 1.2. ...
The Lage team has barely slowed down during the pandemic as evidenced by the mass production of 1.2 billion human excitatory neurons by @gretapinta and @JacquiMMartn1 to study the biological mechanisms that are affected in neuropsychiatric disease.. ...
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Machtens, J. P.; Kortzak, D.; Lansche, C.; Leinenweber, A.; Kilian, P.; Begemann, B.; Zachariae, U.; Ewers, D.; de Groot, B. L.; Briones, R. et al.; Fahlke, C.: Mechanisms of anion conduction by coupled glutamate transporters. Cell 160 (3), pp. 542 - 553 (2015 ...
Excitatory amino acid carrier 1 (EAAC1) is an important subtype of excitatory amino acid transporters (EAATs) and is the route for neuronal cysteine uptake. CoCl 2 is not only a hypoxia-mimetic reagent but also an oxidative stress inducer. Here, we found that CoCl 2 induced significant EAAC1 over...
Genetic polymorphisms in Solute carrier family 1 (glial high affinity glutamate transporter), member 2 (SLC1A2) have been linked with essential tremor. SLC1A2 encodes excitatory amino acid transporter type 2 (EAAT2), which clears glutamate from the synaptic cleft. One postulated mechanism for essential tremor is the over-excitation of glutamatergic olivo-cerebellar climbing fibers, leading to excitotoxic death of Purkinje cells. Other glutamatergic excitatory signals are transmitted to Purkinje cells via parallel fibers of cerebellar granule neurons. Therefore, the expression level of glutamate transporters could be important in essential tremor pathogenesis. Using Western blotting, we compared the expression levels of the two main glutamate transporters in the cerebellar cortex, EAAT1 and EAAT2, in postmortem tissue from 16 essential tremor cases and 13 age-matched controls. We also studied the localization of EAAT1 and EAAT2 using immunohistochemistry in 10 essential tremor cases and 12 controls.
Glutamate excitotoxicity has been implicated in the pathophysiology of epilepsy. Systemic injection of kainic acid (KA) in the rat produces an animal model of human temporal lobe epilepsy. We examined the temporal expression of the sodium-dependent n
EAAC1/EAAT3 is a transporter of glutamate (Glu) present at the post‐synaptic neuronal element, in opposition to the two other main transporters, GLAST/EAAT1 and GLT1/EAAT2, expressed at the excitatory amino acid (EAA) synapse by surrounding astrocytes. Although, in the adult, EAAC1/EAAT3 exhibits a rather low expression level and is considered to make a minor contribution to Glu removal from the synapse, its early expression during brain development, before the astrocytes are functional, suggests that such a neuronal transporter is involved in the developmental effects of EAA and, possibly, in the biosynthesis and trophic role of GABA, which is excitatory in nature in different brain regions during the earlier stages of brain development. This neuronal Glu transporter is considered to have a dual action as it is apparently involved in the neuronal uptake of cysteine, which acts as a key substrate for the synthesis of glutathione, a major anti‐oxidant, because the neurones do not express the Xc-
Glutamate plays an important role in skin barrier signaling. In our previous study, Yokukansan (YKS) affected glutamate receptors in NC/Nga mice and was ameliorated in atopic dermatitis lesions. The aim of this study was to assess the effect of YKS on skin and cultured human keratinocytes. Glutamate concentrations in skin of YKS-treated and nontreated NC/Nga mice were measured. Then, glutamate release from cultured keratinocytes was measured, and extracellular glutamate concentrations in YKS-stimulated cultured human keratinocytes were determined. The mRNA expression levels of NMDA receptor 2D (NMDAR2D) and glutamate aspartate transporter (GLAST) were also determined in YKS-stimulated cultured keratinocytes. The glutamate concentrations and dermatitis scores increased in conventional mice, whereas they decreased in YKS-treated mice. Glutamate concentrations in cell supernatants of cultured keratinocytes increased proportionally to the cell density. However, they decreased dose-dependently with YKS. YKS
The neuronal glutamate transporter EAAC1 contains several conserved acidic amino acids in its transmembrane domain, which are possibly important in catalyzing t
Restoration of Glutamate Transporter Protein (EAAT2) for the treatment of Amyotrophic Lateral Sclerosis (ALS), AD, and PD.. Collaborator: Professor Glenn Lin at Ohio State University. The concentration of glutamate in the synaptic cleft is tightly regulated by the interplay between glutamate release and glutamate clearance. Abnormal glutamate release and/or dysfunction of glutamate clearance can cause over-stimulation of glutamate receptors and result in neuronal injury or death known as excitotoxicity. Excitotoxicity contributes to a number of acute and chronic neurodegenerative diseases. Blocking glutamate receptors and/or reducing glutamate release have been therapeutic strategies for the prevention of excitotoxicity; however, the benefits of these approaches are limited. We have targeted the glial glutamate transporter EAAT2, which is primarily localized in peri-synaptic processes of astrocytes closely associated with excitatory synaptic contacts, and which is responsible for maintaining low ...
Glutamate is the predominant excitatory neurotransmitter in the mammalian central nervous system and extracellular glutamate levels are controlled by a family of transporters known as excitatory amino acid transporters (EAATs). The EAATs transport glutamate and aspartate with similar micromolar affinities and this transport is coupled to the movement of Na(+), K(+), and H(+). The crystal structure of a prokaryotic homologue of the EAATs, aspartate transporter from Pyrococcus horokoshii (Glt(Ph)), has yielded important insights into the architecture of this transporter family. Glt(Ph) is a Na(+)-dependent transporter that has significantly higher affinity for aspartate over glutamate and is not coupled to H(+) or K(+). The highly conserved carboxy-terminal domains of the EAATs and Glt(Ph) contain the substrate and ion binding sites, however, there are a couple of striking differences in this region that we have investigated to better understand the transport mechanism. An arginine residue is in ...
Expression of this gene is affected by vitamin A. The encoded protein of this gene may be associated with the cytoskeleton. A similar protein in rats may play a role in the regulation of cell differentiation. The rat protein binds and inhibits the cell membrane glutamate transporter EAAC1. The expression of the rat gene is upregulated by retinoic acid, which results in a specific reduction in EAAC1-mediated glutamate transport. [provided by RefSeq, Jul 2008 ...
We have recently reported a neuroprotective effect of aspirin concomitant with inhibition of glutamate release in an in vitro model of brain ischemia using rat forebrain slices exposed to OGD.10 We have now used another model of cerebral ischemia consisting of cultured rat cortical neurons exposed to OGD to elucidate further this neuroprotective effect. Our results show that, in cortical neurons, aspirin causes specific protection that is due to inhibition of OGD-induced release of glutamate, by the inhibition of the fall in ATP responsible for the reversal of glutamate uptake systems in cerebral ischemia.. OGD causes cell damage to cortical neurons, as deduced by the release of LDH, the inhibition of MTT reduction, and the staining with propidium iodide. In addition, aspirin inhibits neuronal death induced by OGD, as demonstrated with all 3 of these viability parameters.. The next question we approached concerned the mechanism involved. Although aspirin possesses a wide spectrum of ...
The immune privileged nature of the CNS can make it vulnerable to chronic and latent infections. Little is known about the effects of lifelong brain infections, and thus inflammation, on the neurological health of the host. Toxoplasma gondii is a parasite that can infect any mammalian nucleated cell with average worldwide seroprevalence rates of 30%. Infection by Toxoplasma is characterized by the lifelong presence of parasitic cysts within neurons in the brain, requiring a competent immune system to prevent parasite reactivation and encephalitis. In the immunocompetent individual, Toxoplasma infection is largely asymptomatic, however many recent studies suggest a strong correlation with certain neurodegenerative and psychiatric disorders. Here, we demonstrate a significant reduction in the primary astrocytic glutamate transporter, GLT-1, following infection with Toxoplasma. Using microdialysis of the murine frontal cortex over the course of infection, a significant increase in extracellular ...
Bacigaluppi, M., Russo, G. L., Peruzzotti-Jametti, L., Rossi, S., Sandrone, S., Butti, E., . . . Martino, G. (2016). Neural Stem Cell Transplantation Induces Stroke Recovery by Upregulating Glutamate Transporter GLT-1 in Astrocytes. The Journal of Neuroscience, 36(41), 10529.. Beck, M. H., Haumesser, J. K., Kühn, J., Altschüler, J., Kühn, A. A., & van Riesen, C. (2016). Short- and long-term dopamine depletion causes enhanced beta oscillations in the cortico-basal ganglia loop of parkinsonian rats. Experimental Neurology, 286, 124-136. doi: http://dx.doi.org/10.1016/j.expneurol.2016.10.005.. Huang, C.-W., Chen, Y.-W., Lin, Y.-R., Chen, P.-H., Chou, M.-H., Lee, L.-J., . . . Chen, S.-L. (2016). Conditional Knockout of Breast Carcinoma Amplified Sequence 2 (BCAS2) in Mouse Forebrain Causes Dendritic Malformation via β-catenin. Scientific Reports, 6, 34927. doi: 10.1038/srep34927. Sack, M., Lenz, J. N., Jakovcevski, M., Biedermann, S. V., Falfán-Melgoza, C., Deussing, J., . . . Auer, M. K. ...
TY - ABST. T1 - A functioning glycolysis is important for maintenance of glutamate transport in cultured astrocytes. AU - Schousboe, Arne. AU - Sickmann, Helle Mark. AU - Bak, Lasse Kristoffer. AU - Schousboe, Inger. AU - Bouman, S.D.. AU - Waagepetersen, Helle S.. N1 - Conference code: 3. PY - 2010. Y1 - 2010. KW - Former Faculty of Pharmaceutical Sciences. U2 - 10.1111/j.1471-4159.2009.05927.x. DO - 10.1111/j.1471-4159.2009.05927.x. M3 - Conference abstract in journal. SP - 288. EP - 289. JO - Journal of Neurochemistry. JF - Journal of Neurochemistry. SN - 0022-3042. IS - s1. Y2 - 27 June 2008 through 1 July 2008. ER - ...
Principal Investigator:KONDOH Takeshi, Project Period (FY):1997 - 1999, Research Category:Grant-in-Aid for Scientific Research (B), Section:展開研究, Research Field:Cerebral neurosurgery
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Anti-EAAT1 (GLAST) (ext.)-FITC Antibody (#AGC-021-F) from Alomone Labs is a highly specific rabbit polyclonal Ab directly conjugated to FITC. Ideal for live cell flow cytometry experiments. Lyophilized. Global shipping at room temperature. Your top supplier for glutamate transporter research!
Serine/threonine-protein kinase which is involved in the regulation of a wide variety of ion channels, membrane transporters, cell growth, survival and proliferation. Up-regulates Na(+) channels: SCNN1A/ENAC, K(+) channels: KCNA3/Kv1.3, KCNE1 and KCNQ1, amino acid transporter: SLC6A19, glutamate transporter: SLC1A6/EAAT4, glutamate receptors: GRIA1/GLUR1 and GRIK2/GLUR6, Na(+)/H(+) exchanger: SLC9A3/NHE3, and the Na(+)/K(+) ATPase ...
GLT25D2兔多克隆抗体(ab122192)可与小鼠, 大鼠, 人样本反应并经WB, IHC, ICC/IF实验严格验证。所有产品均提供质保服务,中国75%以上现货。
Glaucoma, a progressive optic neuropathy due to retinal ganglion cell (RGC) degeneration, is one of the leading causes of irreversible blindness. Although glaucoma is often associated with elevated intraocular pressure (IOP), IOP elevation is not detected in a significant subset of glaucomas, such as normal tension glaucoma (NTG). Moreover, in some glaucoma patients, significant IOP reduction does not prevent progression of the disease. Thus, understanding IOP-independent mechanisms of RGC loss is important. Here, we show that mice deficient in the glutamate transporters GLAST or EAAC1 demonstrate spontaneous RGC and optic nerve degeneration without elevated IOP. In GLAST-deficient mice, the glutathione level in Müller glia was decreased; administration of glutamate receptor blocker prevented RGC loss. In EAAC1-deficient mice, RGCs were more vulnerable to oxidative stress. These findings suggest that glutamate transporters are necessary both to prevent excitotoxic retinal damage and to ...
Cortical dysplasia is associated with intractable epilepsy and developmental delay in young children. Recent work with the rat freeze-induced focal cortical dysplasia (FCD) model has demonstrated that hyperexcitability in the dysplastic cortex is due in part to higher levels of extracellular glutamate. Astrocyte glutamate transporters play a pivotal role in cortical maintaining extracellular glutamate concentrations. Here we examined the function of astrocytic glutamate transporters in a FCD model in rats. Neocortical freeze lesions were made in postnatal day (PN) 1 rat pups and whole cell electrophysiological recordings and biochemical studies were performed at PN 21-28. Synaptically evoked glutamate transporter currents in astrocytes showed a near 10-fold reduction in amplitude compared to sham operated controls. Astrocyte glutamate transporter currents from lesioned animals were also significantly reduced when challenged exogenously applied glutamate. Reduced astrocytic glutamate transport ...
TY - JOUR. T1 - The effects of acute intraocular pressure elevation on rat retinal glutamate transport. AU - Holcombe, David J.. AU - Lengefeld, Nadia. AU - Gole, Glen A.. AU - Barnett, Nigel L.. PY - 2008/6/1. Y1 - 2008/6/1. N2 - Purpose: To investigate the relationship between intraocular pressure (IOP), retinal glutamate transport and retinal hypoxia during acute IOP elevations of varying magnitude. Methods: Female Dark Agouti rats were anaesthetized by ketamine/xylazine/ acepromazine (10/5/0.5 mg/kg i.p.). The anterior chamber was cannulated with a 30-gauge needle attached to a saline reservoir. The target IOP (20-120 mmHg, in 10 mmHg increments) was obtained by adjusting the reservoir height. After 10 mins of IOP stabilization, 2 μl of the non-endogenous glutamate transporter substrate, D-aspartate, was injected into the vitreous (final concentration 50 μm), and the elevated IOP maintained for a further 60 mins (total duration of IOP elevation was 70 mins). Glutamate transporter function ...
Glutamate is the primary excitatory neurotransmitter in the mammalian central nervous system. The precise control of extracellular glutamate is crucial for the maintenance of normal synaptic transmission and the prevention of excitotoxicity. High-affinity glutamate transporters ensure termination of glutamatergic neurotransmission and keep the synaptic glutamate concentration below excitotoxic levels. In layer III, a region that is especially prone to cell damage in Alzheimers disease, schizophrenia and epilepsy, and layer V of the medial entorhinal cortex (mEC) effects of blocking glutamate uptake on excitatory synaptic transmission were studied. Extracellular recordings in rat brain slices revealed that application of glutamate uptake inhibitors significantly reduced stimulus-induced negative field potentials in both, layer III and V of the mEC. This effect showed no significant differences in both layers suggesting a similar glutamate regulation in layer III and V. Therefore, only layer III ...
Excitatory amino acid transporters (EAATs) in the CNS maintain extracellular glutamate concentrations below excitotoxic levels and contribute to the clearance o...
ABSTRACT GLUTAMATE TRANSPORT AFFECTS MITOCHONDRIA AND CALCIUM SIGNALING IN ASTROCYTIC PROCESSES UNDER NORMAL AND PATHOLOGICAL CONDITIONS John Charles ODonnell Michael B. Robinson Mitochondria are responsible for synthesis and metabolism of the primary excitatory neurotransmitter, glutamate, which is cleared from synapses via Na+-dependent transporters on astrocytes. Astrocytic clearance of glutamate is required to prevent excitotoxic neuronal death. Mitochondria also participate in calcium signaling in various cell types. Astrocytic calcium signaling is implicated in neurovascular coupling. Glutamate transport and calcium signaling are central to the function of astrocytic processes that are in turn vital for normal brain function. We recently confirmed that mitochondria are present throughout astrocytic processes. Using confocal microscopy and hippocampal slice cultures along with a variety of biochemical assays, we sought to elucidate the physiological and pathological interactions between
Title: Co-Existence of GABA and Glu Transporters in the Central Nervous System. VOLUME: 6 ISSUE: 10. Author(s):Giambattista Bonanno, Luca Raiteri, Silvio Paluzzi, Simona Zappettini, Cesare Usai and Maurizio Raiteri. Affiliation:Department of ExperimentalMedicine; Viale Cembrano 4, 16148 Genoa, Italy.. Keywords:Concept of heterotransporters, reciprocal modulation of GABA and Glu release, GAT-1 heterotransporter, anion channel opening, reversal of EAAT-2, amyotrophic lateral sclerosis. Abstract: Co-localization of transporters able to recapture the released or endogenously synthesized transmitter (homotransporters) and of transporters that can selectively take up transmitters/modulators originating from neighbouring structures (heterotransporters) has been demonstrated to occur within the same axon terminal of several neuronal phenotypes. Activation of terminal heterotransporters invariably leads to the release of the transmitter specific to the terminal. Heterotransporters are also increasingly ...
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Coping with dehydration: sympathetic activation and ...TBOA increased renal SNA (top) and MAP (bottom) in both groups, reflecting effects of endogenously released glutamate in the PVN. Responses to TBOA were significantly greater in EH rats (P | 0.05). Prior microinjection of AP5 decreased renal SNA and MAP in the DH rats and effectively prevented sympathoexcitatory and pressor responses to ...Cited by: 11Publish Year: 2014Author: Megan E. Bardgett, Qing-Hui Chen, Qing Guo, Alfredo S Calderon, Mary Ann Andrade, Glenn Matthew Tone...
The videorecord of GLAST launching is available now on the website of Virtual Institute of Astroparticle physics 1-Glast official video 2-Glast launch...
Buy Gabrion Online! Gabrion is a new chemical compound designed as a structural analog of GABA that is effective in the treatment of partial seizures. Most probably the mechanism of action is related to events modulated through its interaction with a receptor thought to be associated with the L-system amino acid carrier protein.
AGO CLIP Reveals an Activated Network for Acute Regulation of Brain Glutamate Homeostasis in Ischemic Stroke …………… Kobayashi M, Benakis C, Anderson C, Moore MJ, Poon C, Uekawa K, Dyke JP, Fak JJ, Mele A, Park CY, Zhou P, Anrather J, Iadecola C, Darnell RB. Cell Rep. 2019 Jul 23;28(4):979-991.e6. PubMed 00. ...
The Glast Gambit: Hotfix 19.5.7 For those that missed Devstream #85, the cyst cure is aimed to come next week on PC. NOTE: if you were using the ...
TY - JOUR. T1 - Hypoxia-ischemia altered expression of glutamate transporter EAAT1 in neonatal rat brain. AU - Tao, Feng. AU - Zhang, Ling Mei. AU - Sun, Feng Yan. PY - 1999/2/24. Y1 - 1999/2/24. N2 - AIM: To observe altered expression of glutamate transporter EAAT1 after hypoxia-ischemia (H-I) in newborn rat brain. METHODS: Expression levels of EAAT1 were detected with immunohistochemistry method. RESULTS: EAAT1 was a little expressed in cerebral cortex at sham-operated group [(36 ± 10) cells/slice]. Its expression in cerebral cortex increased at 24 h and 48 h following H-I [(314 ± 162) cells/slice and (431 ± 149) cells/slice, respectively], and recovered to control level at 72 h following H-I [(52 ± 8) cells/slice]. The expression of EAAT1 in the ipsilateral cortex to common carotid artery (CCA) ligation was higher than that in the contralateral cortex. CONCLUSION: After H-I, the expression of EAAT1 had a temporal change in cerebral cortex of newborn rat, and was mainly located in the ...
Astrocytes are the site of early dysfunction and damage in Mn neurotoxicity. Astrocytes are the most abundant CNS cells (~50% by volume), and they perform numerous essential functions for normal neuronal activity, such as glutamate uptake, glutamine release, K+ and H+ buffering and volume regulation [36, 75, 76]. Astrocytes accumulate up to 50-fold higher Mn concentrations compared to neurons, thus serving as the main homeostatic and storage site for this metal [75, 77]. The intracellular concentration of Mn in astrocytes is ~50-75 μM where it is an essential cofactor for the astrocyte-specific enzyme glutamine synthetase, which catalyzes the conversion of glutamate to glutamine [78, 79]. The excessive accumulation of Mn in astrocytes mediates neurotoxicity primarily by oxidative stress and impairment of glutamate transporters [80, 81]. Mn toxicity has been shown to cause astrocytic alterations in primate models, and exposure of pathophysiologically relevant Mn concentrations in astrocytes in ...
Clearance of extracellular glutamate is essential for limiting the activity of metabotropic glutamate receptors (mGluRs) at excitatory synapses; however, the relative contribution of transporters found in neuronal and glial membranes to this uptake is poorly understood. Hippocampalinterneurons located at the oriens-alveus border express mGluR1alpha, a metabotropic glutamate receptor that regulates excitability and synaptic plasticity. To determine which glutamate transporters are essential for removing glutamate at these excitatory synapses, we recorded mGluR1-mediated EPSCs from oriens-lacunosum moleculare (O-LM) interneurons in acute hippocampal slices. Stimulation in stratum oriens reliably elicited a slow mGluR1-mediated current in O-LM interneurons if they were briefly depolarized to allow Ca2+ entry before stimulation. Selective inhibition of GLT-1 [for glutamate transporter; EAAT2 (for excitatory amino acid transporter)] with dihydrokainate increased the amplitude of these responses ...
The mechanism of release and the role of l-aspartate as a central neurotransmitter are controversial. A vesicular release mechanism for l-aspartate has been difficult to prove, as no vesicular l-aspartate transporter was identified until it was found that sialin could transport l-aspartate and l-glutamate when reconstituted into liposomes. We sought to clarify the release mechanism of l-aspartate and the role of sialin in this process by combining l-aspartate uptake studies in isolated synaptic vesicles with immunocyotchemical investigations of hippocampal slices. We found that radiolabeled l-aspartate was taken up into synaptic vesicles. The vesicular l-aspartate uptake, relative to the l-glutamate uptake, was twice as high in the hippocampus as in the whole brain, the striatum, and the entorhinal and frontal cortices and was not inhibited by l-glutamate. We further show that sialin is not essential for exocytosis of l-aspartate, as there was no difference in ATP-dependent l-aspartate uptake in ...
During operations, neurosurgeons usually perform multiple temporary occlusions of parental artery, possibly resulting in the neuronal damage. It is generally thought that neuronal damage by cerebral ischemia is associated with extracellular concentrations of the excitatory amino acids. In this study, we measured the dynamics of extracellular glutamate release in 11 vessel occlusion(VO) model to compare between single occlusion and repeated transient occlusions within short interval. Changes in cerebral blood flow were monitored by laser-Doppler flowmetry simultaneously with cortical glutamate level measured by amperometric biosensor. From real time monitoring of glutamate release in 11 VO model, the change of extracellular glutamate level in repeated transient occlusion group was smaller than that of single occlusion group, and the onset time of glutamate release in the second ischemic episode of repeated occlusion group was delayed compared to the first ischemic episode which was similar to that of
We use all-atom MD simulations, combined with patch-clamp electrophysiology and time-resolved fluorescence spectroscopy, to investigate functional dynamics of neurotransmitter transporters and Cl- channels. We developed kinetic state models to explain the functional coupling of secondary active glutamate transport and channel-like anion conduction in EAAT glutamate transporters (1-3), and advanced noise analysis techniques to measure unitary properties of transporter-associated channels (4). Using stopped-flow fluorescence recordings, we identified an induced-fit substrate binding mechanism in EAATs (4). The prokaryotic EAAT homolog GltPh is the founding member of the group of transporters with an elevator transport mechanism, and we used essential dynamics sampling to simulate the inward-outward transition path (5). We identified the Cl- permeation pathway and Cl- conduction mechanism in EAATs (5,6) using Computational Electrophysiology, a simulation technique for all-atom MD simulations of ...
BACKGROUND: Elevated levels of oncostatin M (OSM), an interleukin-6 cytokine family member, have been observed in HIV-1-associated neurocognitive disorders (HAND) and Alzheimers disease. However, the function of OSM in these disease conditions is unclear. Since deficient glutamate uptake by astrocytes is instrumental in HAND-associated neurotoxicity, we hypothesized that OSM impairs glutamate uptake in astrocytes and thereby promotes neuronal excitotoxicity. METHODS: Primary cultures of mouse cortical astrocytes, neurons, microglia, and BV2 cell line were used. The expression of glutamate transporters (GLAST/EAAT1 and GLT-1/EAAT2) was investigated using real-time PCR and Western blot, and their activity was assessed by measuring (3)H-D-aspartate uptake. Neuronal toxicity was measured using the colorimetric MTT (3-(4,5-dimethylthiazol-2-yl-) 2,5-diphenyltetrazolium bromide) assay and immunocytochemistry. A chimeric HIV-1 that infects murine cells (EcoHIV/NL4-3-GFP virus (EcoHIV)) was used to ...
The dopamine (DAT), serotonin (SERT), and norepinephrine (NET) transporters, which are collectively referred to as monoamine transporters (MATs), play significant roles in regulating the neuronal response to these neurotransmitters
The overall goal of this research project is to develop an analytical procedure capable of measuring in situ extracellular glutamate levels in real-time during neurophysiological experiments. Such a system was successfully developed under this grant. This system is capable of measuring extracellular glutamate released from neurons following potassium evoked depolarization.*GLUTAMIC ACID
GRM5 - GRM5 (untagged)-Human glutamate receptor, metabotropic 5 (GRM5), transcript variant a available for purchase from OriGene - Your Gene Company.