Enzymes that catalyze the formation of a carbon-carbon double bond by the elimination of AMMONIA. EC 4.3.1.
A class of traumatic stress disorders with symptoms that last more than one month. There are various forms of post-traumatic stress disorder, depending on the time of onset and the duration of these stress symptoms. In the acute form, the duration of the symptoms is between 1 to 3 months. In the chronic form, symptoms last more than 3 months. With delayed onset, symptoms develop more than 6 months after the traumatic event.
A quantitative method of combining the results of independent studies (usually drawn from the published literature) and synthesizing summaries and conclusions which may be used to evaluate therapeutic effectiveness, plan new studies, etc., with application chiefly in the areas of research and medicine.
An anxiety disorder characterized by recurrent, persistent obsessions or compulsions. Obsessions are the intrusive ideas, thoughts, or images that are experienced as senseless or repugnant. Compulsions are repetitive and seemingly purposeful behavior which the individual generally recognizes as senseless and from which the individual does not derive pleasure although it may provide a release from tension.
A direct form of psychotherapy based on the interpretation of situations (cognitive structure of experiences) that determine how an individual feels and behaves. It is based on the premise that cognition, the process of acquiring knowledge and forming beliefs, is a primary determinant of mood and behavior. The therapy uses behavioral and verbal techniques to identify and correct negative thinking that is at the root of the aberrant behavior.
Antibiotic substance produced by Streptomyces garyphalus.
A method for extinguishing anxiety by a saturation exposure to the feared stimulus situation or its substitute.
Works about clinical trials that involve at least one test treatment and one control treatment, concurrent enrollment and follow-up of the test- and control-treated groups, and in which the treatments to be administered are selected by a random process, such as the use of a random-numbers table.
Enzymes that catalyze the first step leading to the oxidation of succinic acid by the reversible formation of succinyl-CoA from succinate and CoA with the concomitant cleavage of ATP to ADP (EC 6.2.1.5) or GTP to GDP (EC 6.2.1.4) and orthophosphate. Itaconate can act instead of succinate and ITP instead of GTP.EC 6.2.1.-.
The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli.
Enzymes that catalyze the formation of acyl-CoA derivatives. EC 6.2.1.
Databases containing information about PROTEINS such as AMINO ACID SEQUENCE; PROTEIN CONFORMATION; and other properties.
S-Acyl coenzyme A. Fatty acid coenzyme A derivatives that are involved in the biosynthesis and oxidation of fatty acids as well as in ceramide formation.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Enzymes which transfer coenzyme A moieties from acyl- or acetyl-CoA to various carboxylic acceptors forming a thiol ester. Enzymes in this group are instrumental in ketone body metabolism and utilization of acetoacetate in mitochondria. EC 2.8.3.
Cellular release of material within membrane-limited vesicles by fusion of the vesicles with the CELL MEMBRANE.
A class of large neuroglial (macroglial) cells in the central nervous system - the largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the BLOOD-BRAIN BARRIER. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with MICROGLIA) respond to injury.
GRAY MATTER situated above the GYRUS HIPPOCAMPI. It is composed of three layers. The molecular layer is continuous with the HIPPOCAMPUS in the hippocampal fissure. The granular layer consists of closely arranged spherical or oval neurons, called GRANULE CELLS, whose AXONS pass through the polymorphic layer ending on the DENDRITES of PYRAMIDAL CELLS in the hippocampus.
Pinched-off nerve endings and their contents of vesicles and cytoplasm together with the attached subsynaptic area of the membrane of the post-synaptic cell. They are largely artificial structures produced by fractionation after selective centrifugation of nervous tissue homogenates.
A non-essential amino acid naturally occurring in the L-form. Glutamic acid is the most common excitatory neurotransmitter in the CENTRAL NERVOUS SYSTEM.
Specialized junctions at which a neuron communicates with a target cell. At classical synapses, a neuron's presynaptic terminal releases a chemical transmitter stored in synaptic vesicles which diffuses across a narrow synaptic cleft and activates receptors on the postsynaptic membrane of the target cell. The target may be a dendrite, cell body, or axon of another neuron, or a specialized region of a muscle or secretory cell. Neurons may also communicate via direct electrical coupling with ELECTRICAL SYNAPSES. Several other non-synaptic chemical or electric signal transmitting processes occur via extracellular mediated interactions.
The communication from a NEURON to a target (neuron, muscle, or secretory cell) across a SYNAPSE. In chemical synaptic transmission, the presynaptic neuron releases a NEUROTRANSMITTER that diffuses across the synaptic cleft and binds to specific synaptic receptors, activating them. The activated receptors modulate specific ion channels and/or second-messenger systems in the postsynaptic cell. In electrical synaptic transmission, electrical signals are communicated as an ionic current flow across ELECTRICAL SYNAPSES.
The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.
Chemical substances that attract or repel cells. The concept denotes especially those factors released as a result of tissue injury, microbial invasion, or immunologic activity, that attract LEUKOCYTES; MACROPHAGES; or other cells to the site of infection or insult.
Movement characteristics of SPERMATOZOA in a fresh specimen. It is measured as the percentage of sperms that are moving, and as the percentage of sperms with productive flagellar motion such as rapid, linear, and forward progression.
Effective in the initiation of protein synthesis. The initiating methionine residue enters the ribosome as N-formylmethionyl tRNA. This process occurs in Escherichia coli and other bacteria as well as in the mitochondria of eucaryotic cells.
The movement of leukocytes in response to a chemical concentration gradient or to products formed in an immunologic reaction.
Filamentous proteins that are the main constituent of the thin filaments of muscle fibers. The filaments (known also as filamentous or F-actin) can be dissociated into their globular subunits; each subunit is composed of a single polypeptide 375 amino acids long. This is known as globular or G-actin. In conjunction with MYOSINS, actin is responsible for the contraction and relaxation of muscle.
The motor activity of the GASTROINTESTINAL TRACT.
Books used in the study of a subject that contain a systematic presentation of the principles and vocabulary of a subject.
They are oval or bean shaped bodies (1 - 30 mm in diameter) located along the lymphatic system.
The interstitial fluid that is in the LYMPHATIC SYSTEM.
Transfer of a neoplasm from its primary site to lymph nodes or to distant parts of the body by way of the lymphatic system.
Protrusion of the rectal mucous membrane through the anus. There are various degrees: incomplete with no displacement of the anal sphincter muscle; complete with displacement of the anal sphincter muscle; complete with no displacement of the anal sphincter muscle but with herniation of the bowel; and internal complete with rectosigmoid or upper rectum intussusception into the lower rectum.
The homogeneous mixtures formed by the mixing of a solid, liquid, or gaseous substance (solute) with a liquid (the solvent), from which the dissolved substances can be recovered by physical processes. (From Grant & Hackh's Chemical Dictionary, 5th ed)
A mitosporic fungal genus and an anamorphic form of Arthroderma. Various species attack the skin, nails, and hair.
Fungal infection of keratinized tissues such as hair, skin and nails. The main causative fungi include MICROSPORUM; TRICHOPHYTON; and EPIDERMOPHYTON.
A mixture of mostly avermectin H2B1a (RN 71827-03-7) with some avermectin H2B1b (RN 70209-81-3), which are macrolides from STREPTOMYCES avermitilis. It binds glutamate-gated chloride channel to cause increased permeability and hyperpolarization of nerve and muscle cells. It also interacts with other CHLORIDE CHANNELS. It is a broad spectrum antiparasitic that is active against microfilariae of ONCHOCERCA VOLVULUS but not the adult form.
A family of ascomycetous fungi, order Onygenales, characterized by smooth ascospores. Genera in the family include Arthroderma, Keratinomyces, and Ctenomyces. Several well-known anamorphic forms are parasitic upon the skin.
Isocoumarins found in ASPERGILLUS OCHRACEUS and other FUNGI. Ochratoxin contaminated FOOD has been responsible for cases of FOODBORNE DISEASES.
A mitosporic Trichocomaceae fungal genus that develops fruiting organs resembling a broom. When identified, teleomorphs include EUPENICILLIUM and TALAROMYCES. Several species (but especially PENICILLIUM CHRYSOGENUM) are sources of the antibiotic penicillin.
Antibiotic and mycotoxin from Aspergillus niveus and Penicillium citrinum.
An amino acid that, as the D-isomer, is the defining agonist for the NMDA receptor subtype of glutamate receptors (RECEPTORS, NMDA).
A class of ionotropic glutamate receptors characterized by affinity for N-methyl-D-aspartate. NMDA receptors have an allosteric binding site for glycine which must be occupied for the channel to open efficiently and a site within the channel itself to which magnesium ions bind in a voltage-dependent manner. The positive voltage dependence of channel conductance and the high permeability of the conducting channel to calcium ions (as well as to monovalent cations) are important in excitotoxicity and neuronal plasticity.
An imperfect fungus present on most agricultural seeds and often responsible for the spoilage of seeds in bulk storage. It is also used in the production of fermented food or drink, especially in Japan.
A class of ionotropic glutamate receptors characterized by their affinity for the agonist AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid).
Drugs that bind to and activate excitatory amino acid receptors.
A plant species of the genus IPOMOEA, family CONVOLVULACEAE. Some cultivars are sweet and edible whereas bitter varieties are a source of SAPONINS. This sweet potato is sometimes referred to as a yam (DIOSCOREA).
Drugs that bind to but do not activate excitatory amino acid receptors, thereby blocking the actions of agonists.

Low resting potential and postnatal upregulation of NMDA receptors may cause Cajal-Retzius cell death. (1/2269)

Using in situ patch-clamp techniques in rat telencephalic slices, we have followed resting potential (RP) properties and the functional expression of NMDA receptors in neocortical Cajal-Retzius (CR) cells from embryonic day 18 to postnatal day 13, the time around which these cells normally disappear. We find that throughout their lives CR cells have a relatively depolarized RP (approximately -50 mV), which can be made more hyperpolarized (approximately -70 mV) by stimulation of the Na/K pump with intracellular ATP. The NMDA receptors of CR cells are subjected to intense postnatal upregulation, but their similar properties (EC50, Hill number, sensitivity to antagonists, conductance, and kinetics) throughout development suggest that their subunit composition remains relatively homogeneous. The low RP of CR cells is within a range that allows for the relief of NMDA channels from Mg2+ blockade. Our findings are consistent with the hypothesis that CR cells may degenerate and die subsequent to uncontrolled overload of intracellular Ca2+ via NMDA receptor activation by ambient glutamate. In support of this hypothesis we have obtained evidence showing the protection of CR cells via in vivo blockade of NMDA receptors with dizocilpine.  (+info)

Activity-dependent metaplasticity of inhibitory and excitatory synaptic transmission in the lamprey spinal cord locomotor network. (2/2269)

Paired intracellular recordings have been used to examine the activity-dependent plasticity and neuromodulator-induced metaplasticity of synaptic inputs from identified inhibitory and excitatory interneurons in the lamprey spinal cord. Trains of spikes at 5-20 Hz were used to mimic the frequency of spiking that occurs in network interneurons during NMDA or brainstem-evoked locomotor activity. Inputs from inhibitory and excitatory interneurons exhibited similar activity-dependent changes, with synaptic depression developing during the spike train. The level of depression reached was greater with lower stimulation frequencies. Significant activity-dependent depression of inputs from excitatory interneurons and inhibitory crossed caudal interneurons, which are central elements in the patterning of network activity, usually developed between the fifth and tenth spikes in the train. Because these interneurons typically fire bursts of up to five spikes during locomotor activity, this activity-dependent plasticity will presumably not contribute to the patterning of network activity. However, in the presence of the neuromodulators substance P and 5-HT, significant activity-dependent metaplasticity of these inputs developed over the first five spikes in the train. Substance P induced significant activity-dependent depression of inhibitory but potentiation of excitatory interneuron inputs, whereas 5-HT induced significant activity-dependent potentiation of both inhibitory and excitatory interneuron inputs. Because these metaplastic effects are consistent with the substance P and 5-HT-induced modulation of the network output, activity-dependent metaplasticity could be a potential mechanism underlying the coordination and modulation of rhythmic network activity.  (+info)

Ischemic tolerance in murine cortical cell culture: critical role for NMDA receptors. (3/2269)

Murine cortical cultures containing both neurons and glia (days in vitro 13-15) were exposed to periods of oxygen-glucose deprivation (5-30 min) too brief to induce neuronal death. Cultures "preconditioned" by sublethal oxygen-glucose deprivation exhibited 30-50% less neuronal death than controls when exposed to a 45-55 min period of oxygen-glucose deprivation 24 hr later. This preconditioning-induced neuroprotection was specific in that neuronal death induced by exposure to excitotoxins or to staurosporine was not attenuated. Neuroprotection was lost if the time between the preconditioning and severe insult were decreased to 7 hr or increased to 72 hr and was blocked if the NMDA antagonist 100 microM 3-((D)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid was applied during the preconditioning insult. This was true even if the duration of preconditioning was increased as far as possible (while still remaining sublethal). A similar preconditioning effect was also produced by sublethal exposure to high K+, glutamate, or NMDA but not to kainate or trans-1-aminocyclopentane-1, 3-dicarboxylic acid.  (+info)

Voltage-dependent properties of dendrites that eliminate location-dependent variability of synaptic input. (4/2269)

We examined the hypothesis that voltage-dependent properties of dendrites allow for the accurate transfer of synaptic information to the soma independent of synapse location. This hypothesis is motivated by experimental evidence that dendrites contain a complex array of voltage-gated channels. How these channels affect synaptic integration is unknown. One hypothesized role for dendritic voltage-gated channels is to counteract passive cable properties, rendering all synapses electrotonically equidistant from the soma. With dendrites modeled as passive cables, the effect a synapse exerts at the soma depends on dendritic location (referred to as location-dependent variability of the synaptic input). In this theoretical study we used a simplified three-compartment model of a neuron to determine the dendritic voltage-dependent properties required for accurate transfer of synaptic information to the soma independent of synapse location. A dendrite that eliminates location-dependent variability requires three components: 1) a steady-state, voltage-dependent inward current that together with the passive leak current provides a net outward current and a zero slope conductance at depolarized potentials, 2) a fast, transient, inward current that compensates for dendritic membrane capacitance, and 3) both alpha amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid- and N-methyl-D-aspartate-like synaptic conductances that together permit synapses to behave as ideal current sources. These components are consistent with the known properties of dendrites. In addition, these results indicate that a dendrite designed to eliminate location-dependent variability also actively back-propagates somatic action potentials.  (+info)

NMDA-dependent currents in granule cells of the dentate gyrus contribute to induction but not permanence of kindling. (5/2269)

Single-electrode voltage-clamp techniques and bath application of the N-methyl-D-aspartate (NMDA) receptor antagonist 2-amino-5-phosphonovaleric acid (APV) were used to study the time course of seizure-induced alterations in NMDA-dependent synaptic currents in granule cells of the dentate gyrus in hippocampal slices from kindled and normal rats. In agreement with previous studies, granule cells from kindled rats examined within 1 wk after the last of 3 or 30-35 generalized tonic-clonic (class V) seizures demonstrated an increase in the NMDA receptor-dependent component of the perforant path-evoked synaptic current. Within 1 wk of the last kindled seizure, NMDA-dependent charge transfer underlying the perforant path-evoked current was increased by 63-111% at a holding potential of -30 mV. In contrast, the NMDA-dependent component of the perforant-evoked current in granule cells examined at 2.5-3 mo after the last of 3 or 90-120 class V seizures did not differ from age-matched controls. Because the seizure-induced increases in NMDA-dependent synaptic currents declined toward control values during a time course of 2.5-3 mo, increases in NMDA-dependent synaptic transmission cannot account for the permanent susceptibility to evoked and spontaneous seizures induced by kindling. The increase in NMDA receptor-dependent transmission was associated with the induction of kindling but was not responsible for the maintenance of the kindled state. The time course of alterations in NMDA-dependent synaptic current and the dependence of the progression of kindling and kindling-induced mossy fiber sprouting on repeated NMDA receptor activation are consistent with the possibility that the NMDA receptor is part of a transmembrane signaling pathway that induces long-term cellular alterations and circuit remodeling in response to repeated seizures, but is not required for permanent seizure susceptibility in circuitry altered by kindling.  (+info)

Distinct populations of NMDA receptors at subcortical and cortical inputs to principal cells of the lateral amygdala. (6/2269)

Fear conditioning involves the transmission of sensory stimuli to the amygdala from the thalamus and cortex. These input synapses are prime candidates for sites of plasticity critical to the learning in fear conditioning. Because N-methyl-D-aspartate (NMDA)-dependent mechanisms have been implicated in fear learning, we investigated the contribution of NMDA receptors to synaptic transmission at putative cortical and thalamic inputs using visualized whole cell recording in amygdala brain slices. Whereas NMDA receptors are present at both of these pathways, differences were observed. First, the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-receptor-mediated component of the synaptic response, relative to the NMDA component, is smaller at thalamic than cortical input synapses. Second, thalamic NMDA responses are more sensitive to Mg2+. These findings suggest that there are distinct populations of NMDA receptors at cortical and thalamic inputs to the lateral amygdala. Differences such as these might underlie unique contributions of the two pathways to fear conditioning.  (+info)

NMDA receptor characterization and subunit expression in rat cultured mesencephalic neurones. (7/2269)

1. NMDA-induced changes in free intracellular Ca2+ concentration ([Ca2+]i) were determined in individual cultured rat mesencephalic neurones by the fura-2 method. mRNA expression encoding NMDA receptor subunits (NR1, NR2A-D) was examined by RT-PCR. 2. NMDA (1-100 microM, plus 10 microM glycine) induced a concentration-dependent increase in [Ca2+]i (EC50 = 5.7 microM). The effect of NMDA was virtually insensitive to tetrodotoxin (0.3 microM) and nitrendipine (1 microM), but dependent on extracellular Ca2+. 5,7-Dichlorokynurenic acid (10 microM), a specific antagonist at the glycine binding site on the NMDA receptor, abolished the NMDA response. 3. Memantine, an open-channel blocker, and ifenprodil, a preferential non-competitive NR1/NR2B receptor antagonist diminished the NMDA effect with an IC50 value of 0.17 and 1 microM, respectively. Ethanol at 50 and 100 mM caused about 25 and 45%-inhibition, respectively. 4. Agarose gel analysis of the PCR products followed by ethidium bromide fluorescence or CSPD chemiluminescence detection revealed an almost exclusive expression of the NR1 splice variants lacking exon (E) 5 and E22. The 3' splice form without both E21 and E22 exceeded that containing E21 by approximately 4 fold. The relative amounts of NR2A, NR2B, NR2C corresponded to approximately 1:2:1. NR2D mRNA was also detectable. 5. In conclusion, mesencephalic neurones bear ethanol-sensitive NMDA receptors which might be involved in the development of ethanol dependence and withdrawal. The high affinity of NMDA to this receptor, its sensitivity to ifenprodil and memantine may suggest that the mesencephalic NMDA receptor comprises the NR1 splice variant lacking E5, NR2B, and NR2C, respectively.  (+info)

Lack of interaction between nitric oxide and the redox modulatory site of the NMDA receptor. (8/2269)

1. The inhibitory effects of nitric oxide (NO) on N-methyl-D-aspartate (NMDA) receptor function have been proposed to be mediated via the interaction of this gas with a redox-sensitive thiol moiety on the receptor. Here, we evaluated this suggested mechanism by examining the actions of various NO donors on native neuronal receptors as well as in wild-type and cysteine-mutated recombinant NMDA receptors expressed in Chinese hamster ovary (CHO) cells. 2. The NO donor N-ethyl-2-(1-ethyl-2-hydroxy-2-nitrosohydraxino)ethanamine (NOC-12; 100 microM) produced a rapid and readily reversible inhibition of whole-cell currents induced by NMDA (30 microM) in cultured cortical neurons. The inhibition was apparent at all holding potentials, though a more pronounced block was observed at negative voltages. The effects of NOC-12 disappeared when the donor was allowed to expire. A similar receptor block was observed with another NO-releasing agent, S-nitroso-N-acetylpenicillamine (SNAP; 1 mM). 3. The blocking effects of NO released by SNAP, 3-morpholinosydnonimine (SIN-1; 1 mM), and 3-[2-hydroxy-1-(1-methylethyl)-2-nitrosohydrazino]-1-propanamin e (NOC-5; 100 microM) on currents mediated by recombinant NRI/NR2B receptors were virtually indistinguishable from those observed on native receptors. Furthermore, mutating cysteines 744 and 798 of NR1, which constitute the principal redox modulatory site of the NR1/NR2B receptor configuration, did not affect the inhibition produced by NO. 4. The NR2A subunit may contribute its own redox-sensitive site. However, the effects of NO on NR1/NR2A receptors were very similar to those seen for all other receptor configurations evaluated. Hence, we conclude that NO does not exert its inhibition of NMDA-induced responses via a modification of any of the previously described redox-sensitive sites on the receptor.  (+info)

PubMed journal article: Glutamate induces the production of reactive oxygen species in cultured forebrain neurons following NMDA receptor activation. Download Prime PubMed App to iPhone, iPad, or Android
Several genes encoding proapoptotic proteins also elevated expression right after NMDA injection: Amounts of Stat1 mRNA were significantly improved at 24 h, and caspase one mRNA was threefold and fourfold elevated in contrast to controls at 24 h and 48 h, respectively. In contrast, monocyte chemotactic protein 1 , a cytokine involved with recruiting white blood cells to websites of infection or inflammation , was similarly expressed from the NMDA and PBS handled retinas, despite the fact that a tendency for greater expression was detected in NMDA retinas at 24 h right after injection. Activation of a number of these molecules immediately after NMDA injection was also detecinhibitors on the protein level with western blotting . At 24 h soon after injection, we found strongly elevated levels of phospho STAT3, STAT3, phospho STAT1, and STAT1 from the NMDA taken care of retinas compared on the PBS injected controls. On top of that, expression of glial fibrillary acidic protein along with the proform ...
Research proven bioactive human Gas-1 Recombinant Protein mediates the antiapoptotic effect of VEGF. In contrast, Gas1 is induced in hippocampal neurons after NMDA exposure but functions as a proapoptotic effector of NMDA mediated excitotoxicity. Gas1 exhibits a range of developmental actions including either promoting or inhibiting growth and differentiation of somite, limb, cerebellar, and eye tissues
N-Metil-D-aspartinska kiselina (N-metil-D-aspartat, NMDA) je aminokiselinski derivat koji deluje kao specifični agonist NMDA receptora. NMDA oponaša dejstvo glutamata, neurotransmitera koji je endogeni ligand tog receptora. Za razliju od glutamata, NMDA se jedino vezuje za i reguliše NMDA receptore, i nema efekta na druge tipove glutamatnih receptora (kao što su AMPA i kainatni). NMDA receptori su posebno važni kad postanu prekomerno aktivni tokom povlačenja alkohola, a to uzrokuje simptome poput agitacije, i u nekim slučajevima epileptičke napade. ...
Cessation of chronic ethanol consumption can increase the sensitivity of the brain to excitotoxic damages. Cannabinoids have been proposed as neuroprotectants in different models of neuronal injury, but their effect have never been investigated in a context of excitotoxicity after alcohol cessation. Here we examined the effects of the pharmacological activation/inhibition of the endocannabinoid system in an in vitro model of chronic ethanol exposure and withdrawal followed by an excitotoxic challenge. Ethanol withdrawal increased N-methyl-D-aspartate (NMDA)-evoked neuronal death, probably by altering the ratio between GluN2A and GluN2B NMDA receptor subunits. The stimulation of the endocannabinoid system with the cannabinoid agonist HU-210 decreased NMDA-induced neuronal death exclusively in ethanol-withdrawn neurons. This neuroprotection could be explained by a decrease in NMDA-stimulated calcium influx after the administration of HU-210, found exclusively in ethanol-withdrawn neurons. By contrast, the
The phosphorylation of Amyloid Precursor Protein (APP) at Thr668 plays a key role in APP metabolism that is highly relevant to AD. The c-Jun-N-terminal kinase (JNK), glycogen synthase kinase-3β (GSK-3β) and cyclin-dependent kinase 5 (Cdk5) can all be responsible for this phosphorylation. These kinases are activated by excitotoxic stimuli fundamental hallmarks of AD. The exposure of cortical neurons to a high dose of NMDA (100 μM) for 30-45 led to an increase of P-APP Thr668. During NMDA stimulation APP hyperphosphorylation has to be assigned to GSK-3β activity, since addition of L803-mts, a substrate competitive inhibitor of GSK-3β reduced APP phosphorylation induced by NMDA. On the contrary, inhibition of JNK and Cdk5 with D-JNKI1 and Roscovitine respectively did not prevent NMDA-induced P-APP increase. These data show a tight connection, in excitotoxic conditions, between APP metabolism and the GSK-3β signaling pathway.
Stroke is an acute brain health issue which causes neuronal damage which has currently no safe and effective neuroprotective treatment approaches. Immediately following a stroke, the brain tissue loses blood perfusion and the center of the infarct deteriorates quickly. This then causes milder ischemia and many brain cells or neurons will result in delayed death which can take up to several hours or even days. Research studies show that the mechanism of cell death is mainly NMDA receptor-dependent excitotoxicity. In ischemic areas, extracellular glutamate levels increase while preventing glutamate release, synaptic activity, or NMDAR activation which was capable of limiting cell death in a variety of stroke models. Thus, preventing excitotoxicity is an important treatment approach for reducing brain damage and improving patient outcome measures following a stroke, and this has definitely encouraged extensive efforts towards developing NMDA receptor-based stroke treatment approaches over the last ...
INSERM - U. 254 et Universite de Montpellier II, CHR Hopital St. Charles, France. An excitatory amino acid, possibly L-glutamate, which probably acts as a neurotransmitter at the inner hair cell-afferent fiber synapses in the cochlea. In the present study, we have used an electrophysiological approach to investigate at this level the presence of a major type of excitatory amino acid receptor, namely the glutamatergic receptor for which N-methyl-D-aspartate is a selective agonist. Our results show that, when N-methyl-D-aspartate and the antagonist 2-amino-5-phosphonovalerate are perfused through the perilymphatic scalae, they induced, by different mechanisms, a significant reduction of the amplitude of the compound action potential and an increase of the N1 latency, both predominant at high intensity tone burst stimulations. No significant difference was found in the presence or absence of Mg2+ in the artificial perilymph used as a vehicle. A further slight N-methyl-D-aspartate-induced decrease ...
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Bicuculline methiodide (BIC-Mel) (10-100 microM) altered the kinetics of N-methyl-D-aspartate (NMDA) responses in single-channel and whole-cell recordings. The principal effect of BIC-Mel (10-100 microM) on NMDA channels was a dose-dependent decrease in mean channel open time (tau o), accompanied by the introduction of a new closed time (tau B) of 14.0 +/- 3.5 msec (mean +/- standard deviation; n = 14) in closed time distributions, which was independent of BIC-Mel concentration. BIC-Mel (10-100 microM) increased the frequency of NMDA channel opening in a dose-dependent manner, offsetting the decrease in tau o, such that the total time spent in the open state per minute was unchanged, and thus the total charge/min through NMDA channels was unchanged. Similarly, the amplitudes of NMDA whole-cell current responses were not noticeably affected by 10-80 microM BIC-Mel, even though power spectra density analysis of the whole-cell NMDA-stimulated noise revealed changes in the underlying channel ...
In addition to its functions as a neuronal messenger molecule, nitric oxide (NO) has also been implicated in playing a major role in ischemic damage and glutamate neurotoxicity. Using primary cortical cultures from transgenic neuronal NO synthase (NOS) null (nNOS-) mice, we definitively establish NO as a mediator of NMDA and hypoxic neurotoxicity. Neurotoxicity elicited by NMDA is markedly attenuated in nNOS- cortical cultures compared with wild-type cultures. The NOS inhibitor nitro-L-arginine is neuroprotective in wild-type but not nNOS- cultures, confirming the role of nNOS-derived NO in glutamate neurotoxicity. Confirming that the nNOS- cultures lack NMDA-stimulated nNOS activity, NMDA did not stimulate the formation of cGMP in nNOS- cultures, but markedly elevates cGMP in wild-type cultures. Both wild- type and nNOS- cultures are sensitive to toxicity induced by NO donors, indicating that pathways stimulated by NO that result in neuronal cell death are still intact in the transgenic mice. ...
The present study documents that NMDA channel activity may be upregulated or downregulated by remote NMDA receptors, depending on the amount of Na+ and Ca2+ influx. If Na+ influx is blocked, Ca2+ influx induced by the activation of remote NMDA receptors may inhibit NMDA channel gating. However, this inhibitory effect can be overcome by an increase in [Na+]i of ,5 mm. Thus there may be a functional Na+-Ca2+ interaction in the regulation of NMDA channels.. Further detailed investigations document that the effects of Na+ and Ca2+ influx on NMDA channel gating during the activation of remote NMDA receptors cannot be explained simply by an algebraic sum of two opposite effects growing monotonically, because (1) Ca2+ influx required to downregulate NMDA receptors under the condition of no Na+ influx is found to be much smaller than that during NMDA receptor activation under normal conditions; (2) a modest Na+ influx, which produces a much smaller increase in [Na+]i than that during NMDA receptor ...
NMDA receptors are glutamate- and glycine-gated channels that mediate fast excitatory transmission in the central nervous system and are critical to synaptic development, plasticity and integration. They have a rich complement of modulatory sites, which represent important pharmacologic targets. Ifenprodil is a well-tolerated NMDA receptor inhibitor; it is selective for GluN2B-containing receptors; and has neuroprotective effects. The mechanism by which ifenprodil inhibits NMDA receptor responses is not fully understood. The inhibition is incomplete and non-competitive with other known NMDA receptor agonists or modulators, although reciprocal effects have been reported between ifenprodil potency and that of extracellular ligands including glutamate, glycine, zinc, protons and polyamines. Recently, structural studies revealed that ifenprodil binds to a unique site at the interface between the extracellular N-termini of GluN1 and GluN2B subunits supporting the view that interactions with other ...
Expressions of N-methyl-D-aspartate receptors NR2A and NR2B subunit proteins in normal and sulfite-oxidase deficient rats hippocampus: effect of exogenous sulf
Routes of NMDA- and K(+)-stimulated calcium entry in rat cerebellar granule cells.: The routes of Ca2+ entry in response to N-methyl-D-aspartate (NMDA) and K+ d
Erythromycin is used to treat many kinds of infections. Erythromycins are also used to prevent strep infections in patients with a history of rheumatic heart disease who may be allergic to penicillin.. ...
TY - JOUR. T1 - Effect of N-methyl-D,L-aspartate (NMA) on gonadotropin-releasing hormone (GnRH) gene expression in male mice. AU - Wu, T. J.. AU - Gibson, Marie J.. AU - Roberts, James L.. N1 - Funding Information: This project was supported by DK39029 (JLR), NS20335 (MJG) and T32-DK07645 (TJW). The authors wish to thank Dr. Areta Dobrjansky for assistance with the LH RIA, and Dr. Yuhua Sun for helpful discussions and Ms. Alice Elste for reading the manuscript.. PY - 2000/4/17. Y1 - 2000/4/17. N2 - The glutamate analog N-methyl-D,L-aspartate (NMA) affects the regulation of GnRH and LH release in mammals. Several laboratories have reported a rapid and transient increase in GnRH mRNA levels of male rats after NMA injection. Studies employing the simultaneous measurements of nuclear GnRH primary transcript RNA, a reflection of gene transcription, and GnRH mRNA suggest that NMAs effect on GnRH gene expression in the rat is likely due to post-transcriptional regulation. Despite the increasingly ...
Purpose: : During NMDA-induced cell death in the neural retina, there is an elevation of the nuclear isoform of CaMKIIα (CaMKIIαB). This result leads to the question of how CaMKIIαB might be involved in either a cell death or cell survival pathway, for example, in retinal ganglion cells (RGCs). The purpose of this study is to investigate if CaMKIIα regulates BDNF expression in RGCs. Methods: : Highly purified RGCs or dissociated retinal cells were obtained from P6-8 SD rat eyes and treated with glutamate (200-1000uM) for the indicated times. Glutamate cytotoxicity on RGCs and localization of CaMKIIα was determined by cell counting and immunostaining, respectively. To identify the role of CaMKIIα in regulating BDNF expression, CaMKIIαB expression vector was constructed and over-expressed in cells of the RGC-5 cell line, and cell viability was assayed. Specific siRNAs to knock down CaMKIIαB or CaMKIIα were then tested in CaMKIIαB-transfected or non-transfected RGC-5 cells. The siRNAs ...
N-Methyl-D-aspartic acid or N-Methyl-D-aspartate (NMDA) is an amino acid derivative that acts as a specific agonist at the NMDA receptor mimicking the action of glutamate, the neurotransmitter which normally acts at that receptor. Unlike glutamate, NMDA only binds to and regulates the NMDA receptor and has no effect on other glutamate receptors (such as those for AMPA and kainate). NMDA receptors are particularly important when they become overactive during withdrawal from alcohol as this causes symptoms such as agitation and, sometimes, epileptiform seizures. NMDA is a water-soluble synthetic substance that is not normally found in biological tissue. It was first synthesized in the 1960s. NMDA is an excitotoxin (it kills nerve cells by over-exciting them); this trait has applications in behavioral neuroscience research. The body of work utilizing this technique falls under the term lesion studies. Researchers apply NMDA to specific regions of an (animal) subjects brain or spinal cord and ...
Our results support the hypothesis that cholesterol status of neurons is crucial for excitotoxicity since we found that inhibition of cholesterol synthesis prevents NMDA-induced neuronal death. Two different inhibitors of cholesterol synthesis, the inhibitor of Δ14-Δ7 reductase AY9944 and the inhibitor of HMGCoA reductase simvastatin, protect from excitotoxic cell death in pure neuronal cultures (Figures 2 and 3⇑). Both compounds inhibited cholesterol synthesis, but contrary to simvastatin, AY4499 does not inhibit isoprenylation or farnesylation.22 In agreement with results previously reported,10 we found that simvastatin protected against excitotoxicity at nanomolar concentrations and required pretreatments ,2 days to provide neuroprotection.10,11 These 2 observations suggest that the effect of simvastatin on neuroprotection relays on its effect on cholesterol synthesis, because the inhibition of prenylation by statins occurs at higher concentrations and with shorter exposure times than ...
Dai H, Fu Q, Shen Y, Hu W, Zhang Z, Timmerman H, Leurs R, Chen Z. The histamine H3 receptor antagonist clobenpropit enhances GABA release to protect against NMDA-induced excitotoxicity through the cAMP/protein kinase A pathway in cultured cortical neurons. European Journal of Pharmacology. 2007 Jun 1;563(1-3):117-23. PMID 17350613 ...
We report here that brief exposure to 5-50 μM extracellular zinc, comparable to the concentrations estimated to be released normally into synaptic clefts (4), selectively enhanced the phosphorylation of neuronal Src at tyrosine 220 in the SH2 domain, without affecting tyrosine phosphorylation of Fyn. This phosphorylation was accompanied by increases in Src activity, NMDA receptor phosphorylation, and NMDA receptor function (current and excitotoxicity). Drawing on key earlier studies as well as present measurements of [Na+]i in neurons exposed to zinc, we propose that the ability of zinc to induce this up-regulation of Src activity and NMDA receptor function is mediated by inhibition of plasma membrane Na+/K+ ATPase and elevated [Na+]i. Although low concentrations of zinc can potentiate current mediated by certain homomeric NMDA receptor subunit 1 (NR1) splice variants, zinc potentiation of more physiological heteromeric NR1/NR2 receptors was not previously observed (70, 71).. No change in the ...
After an excitotoxic lesion in the postnatal cortex, glial NF-κB is consistently activated at 10 hours after injury, showing its peak at day 1.4 Therefore, when triflusal is orally administered 8 hours after the NMDA injection, it preferentially targets NF-κB induced in glial cells, as the inducible neuronal NF-κB is starting to decrease when triflusal reaches the brain. Glial NF-κB is probably induced by injury-related signals that occur in the degenerating area. They may include reactive oxygen species, produced in excitotoxically damaged cells,44 and the proinflammatory cytokines interleukin-1β and tumor necrosis factor-α, which are expressed by neurons and glial cells in this excitotoxic lesion model, showing a peak of expression at 10 hours after injury.45 On activation, NF-κB translocates to the cell nucleus and modulates the expression of several genes implicated in the development of the glial and inflammatory responses. Target genes containing a NF-κB-binding site include the ...
TY - JOUR. T1 - Na+ occupancy and Mg2+ block of the N-methyl-D-aspartate receptor channel. AU - Zhu, Yongling. AU - Auerbach, Anthony. PY - 2001. Y1 - 2001. N2 - The effect of extracellular and intracellular Na+ on the single-channel kinetics of Mg2+ block was studied in recombinant NR1-NR2B NMDA receptor channels. Na+ prevents Mg2+ access to its blocking site by occupying two sites in the external portion of the permeation pathway. The occupancy of these sites by intracellular, but not extracellular, Na+ is voltage-dependent. In the absence of competing ions, Mg2+ binds rapidly (,108 M-1s-1, with no membrane potential) to a site that is located 0.60 through the electric field from the extracellular surface. Occupancy of one of the external sites by Na+ may be sufficient to prevent Mg2+ dissociation from the channel back to the extracellular compartment. With no membrane potential; and in the absence of competing ions, the Mg2+ dissociation rate constant is ,10 times greater than the Mg2+ ...
N-methyl-D-aspartate receptors activate transcription of c-fos and NGFI-A by distinct phospholipase A2-requiring intracellular signaling pathways.
Lately there has been alot of hype around ketamine for the treatement of depression. There has also been some talks regarding NMDA receptor agonists...
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Background Constitutive and regulated internalization of cell surface proteins has been extensively investigated. The regulated internalization has been characterized as a principal mechanism for...
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Title: New Peptidic Neuroprotectants Against NMDA Neurotoxicity: Syntheses and Biological Evaluations of Linear Complestatin Analogs. VOLUME: 5 ISSUE: 2. Author(s):Ho-Joon Park, Seung-Woo Kim, Young-Gyun Shin, Yun-Jung Kim, Ja-Kyeong Lee, Suk Bin Kong and Sung-Hwa Yoon. Affiliation:Department of Molecular Science and Technology, Ajou University, Suwon, 443-749 South Korea.. Keywords:NMDA, Neurotoxicity, Complestatin, LDH release, 3,5-dichloro-4-hydroxyphenylglycine. Abstract: Linear peptide analogs of complestatin were synthesized via solid phase peptide synthesis and tested in vitro as inhibitors against N-methyl-D-aspartic acid (NMDA) neurotoxicity as possible new peptidic neuroprotectants. While none of the analogs were as potent as the parent compound (IC50 = 2.5 μM), hexamer 11c and heptamer 1c, which contain all D-amino acids, showed modestly potent neuroprotective effects with IC50 values of 23.8 μM and 22.5 μM, respectively. The results indicate that the bicyclic ring structure of ...
DHEA, together with DHEAS, is the most abundant steroid in the blood of young adult humans. Levels in humans decline with age and during certain types of illness or stress. We have found that DHEA(S) can prevent or reduce the neurotoxic actions in the hippocampus of the glutamate agonists N-methyl-d-aspartic acid (NMDA) both in vitro and in vivo or α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainic acid in vitro. Pre-treatment with DHEA (10-100 nM for 6-8 h) protected primary hippocampal cultures from embryonic day 18 (E18) embryos against NMDA-induced toxicity (0.1, 1, 10, and 50 mM). DHEA added either with NMDA (1 mM) or 1 h later had lesser, but still significant, protective actions. DHEAS also reduced NMDA-induced toxicity (1 mM), although the lowest effective dose of DHEAS (100 nM) was higher than that of DHEA (10 nM). DHEA (100 nM) protected cultured neurons against the neurotoxic actions of either AMPA (25 μM) or kainic acid (1 mM) as well. In vivo, s.c. pellets of ...
2In slices, the potencies of the weakly (or non-) transported analogues, N-methyl-D-aspartate (NMDA) and kainate (KA) (EC50 = 40 μM each) were higher than those of the transported amino acids, D- and L-aspartate (EC50 = 250 μM and 300 μM) and D- and L-glutamate (EC50 = 540 μM and 480 μM). Quisqualate (up to 300 μM) failed to increase cyclic GMP levels significantly. The sensitivity of agonist responses to the NMDA receptor antagonist, DL-2-amino-5-phosphonovalerate (APV), was in the order NMDA , L-aspartate , L-glutamate, KA ...
QNZ46 is a NMDA receptor antagonist. QNZ46 inhibits NMDA receptor function in a noncompetitive and voltage-independent manner by an unconventional mechanism that requires binding of glutamate to the GluN2 subunit, but not glycine binding to the GluN1 subunit. QNZ46 could provide an opportunity for the development of pharmacological tools and therapeutic agents that target NMDA receptors at a new site and modulate function by a novel mechanism. NMDA receptors are ionotropic glutamate receptors that mediate excitatory synaptic transmission and have been implicated in several neurological diseases.
Transgenic Huntingtons disease (HD) mice, expressing exon 1 of the human HD gene (lines R6/1 and R6/2), are totally resistant to striatal lesions caused by the NMDA receptor agonist quinolinic acid (QA). Here we show that this resistance develops gradually over time in both R6/1 and R6/2 mice, and that it occurred earlier in R6/2 (CAG-155) than in R6/1 (CAG-115) mice. The development of the resistance coincided with the appearance of nuclear inclusions and with the onset of motor deficits. In the HD mice, hippocampal neurons were also resistant to QA, especially in the CA1 region. Importantly, there was no change in susceptibility to QA in transgenic mice with a normal CAG repeat (CAG-18). R6/1 mice were also resistant to NMDA-, but not to AMPA-induced striatal damage. Interestingly, QA-induced current and calcium influx in striatal R6/2 neurons were not decreased. However, R6/2 neurons had a better capacity to handle cytoplasmic calcium ([Ca2+](c)) overload following OA and could avoid ...
Long-term potentiation of NMDA-receptor-mediated synaptic transmission (NMDAR-LTP) is a little-understood form of plasticity. In the present study, we investigated whether NMDAR-LTP in the dentate gyrus involves recruitment of extrasynaptic NMDARs, because NMDARs are expressed both synaptically and extrasynaptically with evidence for subtype differences at different locations. We show that before induction of NMDAR-LTP, pharmacological inhibition of glutamate transporters resulted in glutamate spillover from the synapse and activation of extrasynaptic NMDARs. After the induction of NMDAR-LTP, such activation of extrasynaptic NMDARs was absent. Activation of extrasynaptic NMDARs after glutamate uptake inhibition also occurred when synaptic NMDARs were inhibited with MK801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo [a,d] cyclohepten-5,10-imine maleate], and this extrasynaptically mediated NMDAR-EPSC was strongly reduced by prior induction of NMDAR-LTP. The extrasynaptic NMDARs were shown to be ...
TY - JOUR. T1 - Hypoxia modulates nitric oxide-induced regulation of NMDA receptor currents and neuronal cell death. AU - Gbadegesin, Muyiwa. AU - Vicini, Stefano. AU - Hewett, Sandra. AU - Wink, David A.. AU - Espey, Michael. AU - Pluta, Ryszard M.. AU - Colton, Carol A.. PY - 1999. Y1 - 1999. N2 - Nitric oxide (NO) released from a new chemical class of donors enhances N-methyl-D-aspartate (NMDA) channel activity. Using whole cell and single- channel patch-clamp techniques, we have shown that (Z)-1-[N(3-ammoniopropyl)- N-(n-propyl)amino]-NO (PAPA-NO) and diethylamine NO, commonly termed NONOates, potentiate the glutamate-mediated response of recombinant rat NMDA receptors(NR1/NR2A) expressed in HEK-293 cells. The overall effect is an increase in both peak and steady-state whole cell currents induced by glutamate. Single-channel studies demonstrate a significant increase in open probability but no change in the mean single-channel open time or mean channel conductance. Reduction in oxygen levels ...
Toxicol Lett. 2011 Sep 10;205(3):336-40. Epub 2011 Jun 24. Chen HH, Lin YR, Chan MH. Source Institute of Pharmacology and Toxicology, Tzu Chi University, 701, Sec. 3, Chung Yang Rd., Hualien 97004, Taiwan. Abstract Toluene, an industrial organic solvent, is voluntarily inhaled as drug of abuse. Because inhibition of N-methyl-d-aspartate (NMDA) receptors is one of…
TY - JOUR. T1 - Neuronal and glial localization of NMDA receptors in the cerebral cortex. AU - Conti, Fiorenzo. AU - Minelli, Andrea. AU - DeBiasi, Silvia. AU - Melone, Marcello. PY - 1997/2. Y1 - 1997/2. N2 - The crucial role of glutamate receptors of the N-methyl-D-aspartate (NMDA) type in many fundamental cortical functions has been firmly established, as has its involvement in several neuropsychiatric diseases, but until recently, very little was known of the anatomical localization of NMDA receptors in the cerebral cortex of mammals. The recent application of molecular biological techniques to the study of NMDA receptors has allowed the production of specific tools, the use of which has much increased our understanding of the localization of NMDA receptors in the cerebral cortex. In particular, immunocytochemical studies on the distribution of cortical NMDA receptors have: 1. Demonstrated the preferential localization of NMDA receptors in dendritic spines, in line with previous work; 2. ...
Polyamine potentiation and inhibition of NMDA-mediated increases of intracellular free Ca2+ in cultured chick cortical neurons. Eur J Pharmacol. 1994 Jan 15; 266(2):107-15 ...
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D-Cycloserine, a partial agonist of the glycine recognition site of the N-methyl- D-aspartate ( NM DA) receptor, may serve as a probe for human cerebral NM DA receptor function. Since NM DA receptors
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Biology of the NMDA Receptor - free book at E-Books Directory. You can download the book or read it online. It is made freely available by its author and publisher.
Sigma-1 (σ1) receptor has been identified as a chaperone protein that interacts with other proteins, such as N-methyl-D-aspartate… Expand ...
Its been a heck of a week, friends. Friday was a trip to the pain management clinic, which -- per usual -- was wholeheartedly depressing. I find that I feel even worse whenever I come out of those appointments because I realize how useless they are. Pain management clinics, that is. Massachusetts as a whole is…
Looking for online definition of N-methyl D-aspartate receptor subtype 2C in the Medical Dictionary? N-methyl D-aspartate receptor subtype 2C explanation free. What is N-methyl D-aspartate receptor subtype 2C? Meaning of N-methyl D-aspartate receptor subtype 2C medical term. What does N-methyl D-aspartate receptor subtype 2C mean?
TY - JOUR. T1 - Endogenous D-serine contributes to NMDA-receptor-mediated light-evoked responses in the vertebrate retina. AU - Gustafson, Eric C.. AU - Stevens, Eric R.. AU - Wolosker, Herman. AU - Miller, Robert F.. N1 - Copyright: Copyright 2009 Elsevier B.V., All rights reserved.. PY - 2007/7. Y1 - 2007/7. N2 - We have combined electrophysiology and chemical separation and measurement techniques with capillary electrophoresis (CE) to evaluate the role of endogenous D-serine as an NMDA receptor (NMDAR) coagonist in the salamander retina. Electrophysiological experiments were carried out using whole cell recordings from retinal ganglion cells and extracellular recordings of the proximal negative response (PNR), while bath applying two D-serine degrading enzymes, including Damino acid oxidase (DAAO) and D-serine deaminase (DsdA). The addition of either enzyme resulted in a significant and rapid decline in the light-evoked responses observed in ganglion cell and PNR recordings. The addition of ...
TY - JOUR. T1 - Pathologically activated neuroprotection via uncompetitive blockade of N-methyl-D-aspartate receptors with fast off-rate by novel multifunctional dimer bis(propyl)-cognitin. AU - Luo, Jialie. AU - Li, Wenming. AU - Zhao, Yuming. AU - Fu, Hongjun. AU - Ma, Dik Lung. AU - Tang, Jing. AU - Li, Chaoying. AU - Peoples, Robert W.. AU - Li, Fushun. AU - Wang, Qinwen. AU - Huang, Pingbo. AU - Xia, Jun. AU - Pang, Yuanping. AU - Han, Yifan. PY - 2010/6/25. Y1 - 2010/6/25. N2 - Uncompetitive N-methyl-D-aspartate (NMDA) receptor antagonists with fast off-rate (UFO) may represent promising drug candidates for various neurodegenerative disorders. In this study, we report that bis(propyl)-cognitin, a novel dimeric acetylcholinesterase inhibitor and γ-aminobutyric acid subtype A receptor antagonist, is such an antagonist of NMDA receptors. In cultured rat hippocampal neurons, we demonstrated that bis-(propyl)-cognitin voltage-dependently, selectively, and moderately inhibited NMDA-activated ...
2-(10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5-ylidene)ethanol - C17H16O, synthesis, structure, density, melting point, boiling point
TITLE AMPA and NMDA receptor with presynaptic short-term plasticity COMMENT AMPA and NMDA receptor conductance using a dual-exponential profile presynaptic short-term plasticity based on Fuhrmann et al. 2002 Implemented by Srikanth Ramaswamy, Blue Brain Project, July 2009 Etay: changed weight to be equal for NMDA and AMPA, gmax accessible in Neuron ENDCOMMENT NEURON { POINT_PROCESS ProbAMPA RANGE tau_r_AMPA, tau_d_AMPA, tau_r_NMDA, tau_d_NMDA RANGE Use, u, Dep, Fac, u0, weight_NMDA RANGE i, i_AMPA, i_NMDA, g_AMPA, g_NMDA, e, gmax, mgVoltageCoeff NONSPECIFIC_CURRENT i POINTER rng } PARAMETER { tau_r_AMPA = 0.2 (ms) : dual-exponential conductance profile tau_d_AMPA = 1.7 (ms) : IMPORTANT: tau_r , tau_d tau_r_NMDA = 0.00000001 (ms) : dual-exponential conductance profile tau_d_NMDA = 0.00000002 (ms) : IMPORTANT: tau_r , tau_d Use = 1.0 (1) : Utilization of synaptic efficacy (just initial values! Use, Dep and Fac are overwritten by BlueBuilder assigned values) Dep = 100 (ms) : relaxation time ...
A series of 2-substituted 3,4-dihydro-2H-1,2-benzothiazine-3-carboxylic acid 1,1-dioxides were synthesized and evaluated for their affinity to the glycine binding site of the N-methyl-d-aspartate (NMDA) receptor. The binding affinity was determined by the displacement of radioligand [(3)H]MDL-105,519 from rat cortical membrane preparations. The most attractive structures in the search for prospective NMDA receptor ligands were identified to be 2-arylcarbonylmethyl substituted 3,4-dihydro-2H-1,2-benzothiazine-3-carboxylic acid 1,1-dioxides. It has been demonstrated for the first time that the replacement of NH group in the ligand by sp(3) CH2 is tolerated. This finding may pave the way for previously unexplored approaches for designing new ligands of the NMDA receptor.
AbstractIn the present study, a twenty-mer antisense oligonucleotide specific for N-methyl-D-aspartate receptor one (ANR1) was applied to striatal neurons in primary cell culture. The ANR1 was found to be specific and nontoxic. Significant reductions in expression of NR1 mRNA and proteins were resulted after a single dose of ANR1 transcripts. Interestingly, there were reductions in total NR1 proteins but two phosphorylated forms of NR1 proteins at serine 896 and 897 residues were not reduced. There was also no change in the pattern of distribution of NR1 immunoreactivity in the striatal neurons. In addition, significant reductions of NMDA-mediated peak inward current were found after application of a higher concentration of ANR1 (20-100 mu M) by patch clamp recordings. The present results indicate that ANR1 is a useful agent in reducing NMIDA receptor functions. The present data thus provide detailed cellular and molecular mechanisms to explain our previous findings of amelioration of motor ...
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Electrical activation of hippocampal neurons can cause calcium influx through different entry sites which may specify nuclear signalling and induction of gene transcription and downstream physiological outputs. Genomic responses initiated by NMDA receptors (NMDARs) are critically dependent on whethe …
Looking for online definition of excitotoxic in the Medical Dictionary? excitotoxic explanation free. What is excitotoxic? Meaning of excitotoxic medical term. What does excitotoxic mean?
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Sigma-Aldrich offers abstracts and full-text articles by [Fernando A Giuliani, Roberto Yunes, Claudia E Mohn, Myriam Laconi, Valeria Rettori, Ricardo Cabrera].
   Forgive me if some of this is repetitive, much of this has been posted on our Ketamine thread, but I felt like it deserved a thread of its own. Ever since I ended up in the ER with a cluster and they gave me I.V. magnesium I have been interested in glutamate toxicity in the brain. I could...
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Olneys lesions Olneys lesions, also known as NMDA receptor antagonist neurotoxicity (NAN), are a form of brain damage caused by high doses of dissociative
As I said, oxytosis, otherwise known as excitotoxicity or glutamate toxicity Hi, justy. I think that what you are experiencing are symptoms of...
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It includes the unusual starter unit methylaspartate. Shindo K, Kamishohara M, Odagawa A, Matsuoka M, Kawai H (July 1993). " ...
It includes the unusual amino acid methylaspartate. Heinzelmann, E.; Berger, S.; Puk, O.; Reichenstein, B.; Wohlleben, W.; ...
Anti-NMDA-receptor encephalitis "N-Methylaspartate - Compound Summary". PubChem Compound. USA: National Center for ...
Church J, Jones MG, Davies SN, Lodge D (June 1989). "Antitussive agents as N-methylaspartate antagonists: further studies". Can ...
... selectively antagonises N-methyl-aspartate (NMA)". Pharmacology, Biochemistry, and Behavior. 24 (1): 23-5. doi:10.1016/0091- ...
... tailoring modification of 3-methyl-aspartate". Journal of Bacteriology. 193 (10): 2647-51. doi:10.1128/jb.00108-11. PMC 3133142 ...
... selectively reduce excitation of central mammalian neurones by N-methyl-aspartate". British Journal of Pharmacology. 79 (2): ...
N-Methylaspartate - Compound Summary". PubChem Compound. USA: National Center for Biotechnology Information. 24. 6. 2005. ...
... and comparisons of the crystal structures of pig cytosolic aspartate aminotransferase and its complex with 2-methylaspartate". ...
... may refer to: L-threo-3-Methylaspartate N-Methyl-D-aspartic acid This set index page lists chemical ...
N-methylaspartate - N-terminus - NADH - NADPH - NaKATPase - Native state - nef gene product - neoplasm protein - Nernst ...
... n-methylaspartate MeSH D12.125.067.500.700 - potassium magnesium aspartate MeSH D12.125.067.750 - glutamic acid MeSH D12.125. ... n-methylaspartate MeSH D12.125.119.170.700 - potassium magnesium aspartate MeSH D12.125.119.270 - carbocysteine MeSH D12.125. ...
... for nickel and carboxyl-methyl aspartate (Co-CMA) for cobalt, which the polyhistidine-tag binds with micromolar affinity. Ernst ...
... a specific agonist at the NMDA receptor L-threo-3-Methylaspartate This set index page lists chemical structure articles ...
... methylaspartate mutase EC 5.4.99.2: methylmalonyl-CoA mutase EC 5.4.99.3: 2-acetolactate mutase EC 5.4.99.4: 2- ...
... methylaspartate ammonia-lyase EC 4.3.1.3: histidine ammonia-lyase EC 4.3.1.4: formiminotetrahydrofolate cyclodeaminase EC 4.3. ...
In enzymology, a methylaspartate mutase (EC 5.4.99.1) is an enzyme that catalyzes the chemical reaction L-threo-3- ... The systematic name of this enzyme class is L-threo-3-methylaspartate carboxy-aminomethylmutase. Other names in common use ... L-threo-3-methylaspartate, and one product, L-glutamate. This enzyme belongs to the family of isomerases, specifically those ... beta-methylaspartate-glutamate mutase, and glutamate isomerase. This enzyme participates in c5-branched dibasic acid metabolism ...
In enzymology, a methylaspartate ammonia-lyase (EC 4.3.1.2) is an enzyme that catalyzes the chemical reaction L-threo-3- ... The systematic name of this enzyme class is L-threo-3-methylaspartate ammonia-lyase (mesaconate-forming). Other names in common ... L-threo-3-methylaspartate, and two products, mesaconate and NH3. This enzyme belongs to the family of lyases, specifically ... methylaspartate ⇌ {\displaystyle \rightleftharpoons } mesaconate + NH3 Hence, this enzyme has one substrate, ...
... is an unusual amino acid formed by glutamate mutase and can be metabolised by methylaspartate ammonia ... Khomyakova, M.; Bukmez, O.; Thomas, L. K.; Erb, T. J.; Berg, I. A. (2011). "A Methylaspartate Cycle in Haloarchaea". Science. ... Methylaspartate cycle). Ogasawara, Y.; Kakinuma, K.; Eguchi, T. (2005). "Involvement of Glutamate Mutase in the Biosynthesis of ...
Methylaspartate may refer to: L-threo-3-Methylaspartate N-Methyl-D-aspartic acid This set index page lists chemical compounds ...
In enzymology, a methylaspartate mutase (EC 5.4.99.1) is an enzyme that catalyzes the chemical reaction L-threo-3- ... The systematic name of this enzyme class is L-threo-3-methylaspartate carboxy-aminomethylmutase. Other names in common use ... L-threo-3-methylaspartate, and one product, L-glutamate. This enzyme belongs to the family of isomerases, specifically those ... beta-methylaspartate-glutamate mutase, and glutamate isomerase. This enzyme participates in c5-branched dibasic acid metabolism ...
"N-Methylaspartate" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical Subject ... This graph shows the total number of publications written about "N-Methylaspartate" by people in Harvard Catalyst Profiles by ... Below are the most recent publications written about "N-Methylaspartate" by people in Profiles. ... Below are MeSH descriptors whose meaning is more general than "N-Methylaspartate". ...
And Comparison Of The Crystal Structures Of Pig Cytosolic Aspartate Aminotransferase And Its Complex With 2-Methylaspartate. ...
Brun, Kathrin A; Heimgartner, Heinz (2005). A new 2H-Azirin-3-amine as a synthon for 2-Methylaspartate. Helvetica Chimica Acta ... Download PDF A new 2H-Azirin-3-amine as a synthon for 2-Methylaspartate. Item availability may be restricted. ... A new 2H-Azirin-3-amine as a synthon for 2-Methylaspartate ...
Hydrogen transfer in the isomerization of .beta.-methylaspartate to glutamate R. G. Eagar Jr., B. G. Baltimore, M. M. Herbst, H ... Mechanism of action of coenzyme B_(12). Hydrogen transfer in the isomerization of β-methylaspartate to glutamate ... The evidence also supports the existence of an intermediate which can partition with similar probabilities to β-methylaspartate ... Use of a mixture of unlabeled and tetradeuterio-,Bmethylaspartate with coenzyme B_(12) dependent β-methylaspartate-glutamate ...
The enzyme studied in this research project is 3‐methylaspartate ammonia lyase (MAL) which catalyses the deamination reaction ... Engineering of 3 methylaspartate ammonia-lyases for biobased adipic acid production. Robin Van Havere ... The assays provided the kinetic constants of the conversion of the natural substrate, 3‐methyl aspartate, by the mutated ... The assays provided the kinetic constants of the conversion of the natural substrate, 3‐methyl aspartate, by the mutated ...
PWY-6728 Methylaspartate cycle * PWY-6969 TCA cycle V (2-oxoglutarate:ferredoxin oxidoreductase) ...
3-methylaspartate ammonia lyase, etc [PMID: 15581566]. These enzymes share a bidomain structure containing a capping domain and ...
N-Methylaspartate. Placebos. Schizophrenia. Amino Acids -- blood. Glycine -- *therapeutic use. Schizophrenia -- *drug therapy. ...
N-Methylaspartate / pharmacology * Neurons / drug effects * Neurons / physiology * Neurons / radiation effects * Patch-Clamp ...
N-Methylaspartate. Excitatory Amino Acid Agonists. Excitatory Amino Acid Agents. Neurotransmitter Agents. Molecular Mechanisms ...
... alpha-methylaspartate; and macrophage inhibitor factor (MIF); among others. A sample or aliquot containing at least one cell ...
L-α-methylaspartate. Masp. L-α-methyl-t-butylglycine. Mtbug. L-α-methylcysteine. Mcys. L-methylethylglycine. Metg. ...
METHYLASPARTATE MUTASE S CHAIN A 137 Clostridium tetanomorphum EC#: 5.4.99.1 IUBMB Gene Name(s): glmS mutS ...
METHYLASPARTATE MUTASE S CHAIN A 137 Clostridium tetanomorphum EC#: 5.4.99.1 IUBMB Gene Name(s): glmS mutS ...
N-Methylaspartate * Rats * Receptors, N-Methyl-D-Aspartate * Receptors, Neurotransmitter / antagonists & inhibitors ...
... are thought to have acquired the unique set of genes for the methylaspartate pathway via a… ... in this instance the intermediate is methylaspartate). Halophilic archaeans, which include Haloarcula marismortui, a model ... in this instance the intermediate is methylaspartate). Halophilic archaeans, which include Haloarcula marismortui, a model ... organism used in scientific research, are thought to have acquired the unique set of genes for the methylaspartate pathway via ...
That metabolic pathway, known as the methylaspartate pathway, represents a unique ... That metabolic pathway, known as the methylaspartate pathway, represents a unique type of anaplerosis (the process of ... are thought to have acquired the unique set of genes for the methylaspartate pathway via a process known as horizontal gene ... replenishing supplies of metabolic intermediates; in this instance the intermediate is methylaspartate). Halophilic archaeans, ...
N-Methyl-Aspartate (NMDA) Receptor Antagonists. Chemical Name: Morphinan, 3-methoxy-17-methyl-, (9α, 13α, 14α)- hydrobromide ...
Involved in the methylaspartate cycle. Catalyzes the reversible cleavage of beta-methylmalyl-CoA to propionyl-CoA and ... "A methylaspartate cycle in haloarchaea.". Khomyakova M., Bukmez O., Thomas L.K., Erb T.J., Berg I.A.. Science 331:334-337(2011) ... "A methylaspartate cycle in haloarchaea.". Khomyakova M., Bukmez O., Thomas L.K., Erb T.J., Berg I.A.. Science 331:334-337(2011) ... "A methylaspartate cycle in haloarchaea.". Khomyakova M., Bukmez O., Thomas L.K., Erb T.J., Berg I.A.. Science 331:334-337(2011) ...
Khomyakova, M., Bükmez, Ö., Thomas, L. K., Erb, T. J., and Berg, I. A. (2011). A methylaspartate cycle in haloarchaea. Science ...
M00740 Methylaspartate cycle. *. M00532 Photorespiration. *. M00013 Malonate semialdehyde pathway, propanoyl-CoA => acetyl-CoA ...
M00740 Methylaspartate cycle. *. M00532 Photorespiration. *. M00013 Malonate semialdehyde pathway, propanoyl-CoA => acetyl-CoA ...
N-methyl aspartate (NMDA), 248, 249, 287, 292 Norepinephrine, 124, 130, 136-137 Nottingham Health Profile, 197 Novantrone, see ...
L-glutamate ↔ L-threo-3-methylaspartate. EC 5.4.99.1. Methyl aspartase. L-threo-3-methylaspartate ↔. mesaconate (2- ... Detailed pathways of glutamate fermentation via 3-methylaspartate [. 37. ]. Glutamate mutase (methylaspartate mutase). ...
N-Methylaspartate - Compound Summary". PubChem Compound. USA: National Center for Biotechnology Information. 24. 6. 2005. ...
Catalytic mechanisms and biocatalytic applications of aspartate and methylaspartate ammonia lyases.. de Villiers M, Puthan ... Engineering methylaspartate ammonia lyase for the asymmetric synthesis of unnatural amino acids. ... Kinetic resolution and stereoselective synthesis of 3-substituted aspartic acids by using engineered methylaspartate ammonia ...
  • The enzyme studied in this research project is 3‐methylaspartate ammonia lyase (MAL) which catalyses the deamination reaction on 3methylaspartic acid. (chalmers.se)
  • This superfamily represents the N-terminal of the enolase and similar structural domains found in several enzymes, such as D-glucarate dehydratases, muconate-lactonizing enzymes, mandelate racemases, d-galactonate dehydratase, O-succinylbenzoate synthases and chlormuconate cycloisomerases, l-Ala-d/l-Glu epimerases, 3-methylaspartate ammonia lyase, etc [ PMID: 15581566 ]. (ebi.ac.uk)
  • In enzymology, a methylaspartate mutase (EC 5.4.99.1) is an enzyme that catalyzes the chemical reaction L-threo-3-methylaspartate ⇌ {\displaystyle \rightleftharpoons } L-glutamate Hence, this enzyme has one substrate, L-threo-3-methylaspartate, and one product, L-glutamate. (wikipedia.org)
  • Use of a mixture of unlabeled and tetradeuterio-,Bmethylaspartate with coenzyme B_(12) dependent β-methylaspartate-glutamate mutase has shown that the hydrogen that migrates becomes one of three equivalent hydrogens during the isomerization. (caltech.edu)
  • PART I. Use of a mixture of non- and tetradeutero-beta-methylaspartate with coenzyme B12 dependent beta-methylaspartate-glutamate mutase has shown that the hydrogen that migrates becomes one of three equivalent hydrogens during the reaction. (caltech.edu)
  • Chih HW and Marsh ENG (2000) Mechanism of glutamate mutase: identification and kinetic competence of acrylate and glycyl radical as intermediates in the rearrangement of glutamate to methylaspartate. (els.net)
  • Glutamate mutase is composed of two separately isolated protein components S and E2, which in the presence of coenzyme B12 assemble to the active holo-glutamate mutase E2S2-B12 that catalyzes the reversible conversion of (S)-glutamate to (2S,3S)-3-methylaspartate. (uni-marburg.de)
  • This reaction has been coupled with methylaspartase, which deaminates (2S,3S)-3-methylaspartate to mesaconate absorbing at 240 nm, to allow activity assays for glutamate mutase by UV-spectrophotometry. (uni-marburg.de)
  • Furthermore, the kinetic constants of (2S,3S)-3-methylaspartate in the reaction of glutamate mutase were determined as Km= 7 ± 0.07 mM, kcat= 0.54 ± 0.06 s-1and kcatKm-1= 77 s-1M-1. (uni-marburg.de)
  • Methylaspartate may refer to: L-threo-3-Methylaspartate N-Methyl-D-aspartic acid This set index page lists chemical compounds articles associated with the same name. (wikipedia.org)
  • Halophilic archaeans, which include Haloarcula marismortui , a model organism used in scientific research, are thought to have acquired the unique set of genes for the methylaspartate pathway via a process known as horizontal gene transfer , in which genes are passed from one species to another. (britannica.com)
  • Two weeks after a unilateral hippocampal aspiration, the 22Na efflux induced by potassium ions, D-glutamate, N-methylaspartate, and kainate is significantly decreased in the contralateral intact hippocampus whereas the effect of L-glutamate is substantially increased. (biomedsearch.com)
  • The effects of potassium ions, N-methylaspartate, and kainate but not of D,L-homocysteate are significantly decreased in slices incubated in the absence of calcium. (biomedsearch.com)
  • Ford, R. M., P. T. Cummings and S. A. Middlebrooks, "Mathematical Model for Combined Response of E. coli to a-Methylaspartate and Nickel Ions," Bacterial Locomotion and Signal Transduction (BLAST) III, Austin, TX, January 12-16, 1995. (virginia.edu)
  • MATHEMATICAL The enzyme -methylaspartase catalyzes the deamination of -methylaspartate [V. Williams and J. Selb. (bartleby.com)
  • Traditional scheme of glutamate fermentation via 3-methylaspartate in C. tetanomorphum . (asm.org)
  • In fact, the ^1H-NMR resonance lines for His18 in the mutant Phe18His showed a dynamic change upon complex formation with a substrate analog, 2-methylaspartate. (nii.ac.jp)
  • To check whether the other compounds acted as reversible inhibitors, a new assay with (2S,3S)-3-methylaspartate and pyruvate as substrates involving glutamate-pyruvate aminotransferase and the NADH-dependent (R)-2-hydroxyglutarate dehydrogenase was developed. (uni-marburg.de)
  • The systematic name of this enzyme class is L-threo-3-methylaspartate carboxy-aminomethylmutase. (wikipedia.org)
  • Van Havere2017, author={Van Havere, Robin}, title={Engineering of 3 methylaspartate ammonia-lyases for biobased adipic acid production}, abstract={The current traditional adipic acid production is a highly polluting process. (chalmers.se)
  • This graph shows the total number of publications written about "N-Methylaspartate" by people in Harvard Catalyst Profiles by year, and whether "N-Methylaspartate" was a major or minor topic of these publication. (harvard.edu)