The Role of Quercetin in Gene Expression of GluR1 Subunit of AMPA Receptors, and NR2A and NR2B Subunits of NMDA Receptors in Kainic Acid Model of Seizure in Mice

2016 ◽  
Vol 19 (5) ◽  
Author(s):  
Sahar Moghbelinejad ◽  
Ghazaleh Mohammadi ◽  
Fatemeh Khodabandehloo ◽  
Reza Najafipour ◽  
Taghi Naserpour ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nmda Receptors ◽  
Kainic Acid ◽  
Ampa Receptors ◽  
Glur1 Subunit

Analysis of the Role of Inhibition in Shaping Responses to Sinusoidally Amplitude-Modulated Signals in the Inferior Colliculus

1998 ◽  
Vol 80 (4) ◽  
pp. 1686-1701 ◽  
Author(s):  
R. Michael Burger ◽  
George D. Pollak
Keyword(s):  
Nmda Receptors ◽  
Inferior Colliculus ◽  
Ampa Receptors ◽  
Phase Locking ◽  
Receptor Blocker ◽  
Response Property ◽  
Medial Superior Olive ◽  
Competitive Antagonist ◽  
Modulated Signals

Burger, R. Michael and George D. Pollak. Analysis of the role of inhibition in shaping responses to sinusoidally amplitude-modulated signals in the inferior colliculus. J. Neurophysiol. 80: 1686–1701, 1998. Neurons in the central nucleus of the inferior colliculus (ICc) typically respond with phase-locked discharges to low rates of sinusoidal amplitude-modulated (SAM) signals and fail to phase-lock to higher SAM rates. Previous studies have shown that comparable phase-locking to SAM occurs in the dorsal nucleus of the lateral lemniscus (DNLL) and medial superior olive (MSO) of the mustache bat. The studies of MSO and DNLL also showed that the restricted phase-locking to low SAM rates is created by the coincidence of phase-locked excitatory and inhibitory inputs that have slightly different latencies. Here we tested the hypothesis that responses to SAM in the mustache bat IC are shaped by the same mechanism that shapes responses to SAM in the two lower nuclei. We recorded responses from ICc neurons evoked by SAM signals before and during the iontophoretic application of several pharmacological agents: bicuculline, a competitive antagonist for γ-aminobutyric acid-A (GABAA) receptors; strychnine, a competitive antagonist for glycine receptors; the GABAB receptor blocker, phaclofen, and the N-methyl-d-aspartate (NMDA) receptor blocker, (−)-2-amino-5-phosphonopentanoic acid (AP5). The hypothesis that inhibition shapes responses to SAM signals in the ICc was not confirmed. In >90% of the ICc neurons tested, the range of SAM rates to which they phase-locked was unchanged after blocking inhibition with bicuculline, strychnine or phaclofen, applied either individually or in combination. We also considered the possibility that faster α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors follow high temporal rates of incoming excitation but that the slower NMDA receptors could follow only lower rates. Thus at higher SAM rates, NMDA receptors might generate a sustained excitation that “smears” the phase-locked excitation generated by the AMPA receptors. The NMDA hypothesis, like the inhibition hypothesis, was also not confirmed. In none of the cells that we tested did the application of AP5 by itself, or in combination with bicuculline, cause an increase in the range of SAM rates that evoked phase-locking. These results illustrate that the same response property, phase-locking restricted to low SAM rates, is formed in more than one way in the auditory brain stem. In the MSO and DNLL, the mechanism is coincidence of phase-locked excitation and inhibition, whereas in ICc the same response feature is formed by a different but unknown mechanism.

scholarly journals Potentiation of Synaptic AMPA Receptors Induced by the Deletion of NMDA Receptors Requires the GluA2 Subunit

2011 ◽  
Vol 105 (2) ◽  
pp. 923-928 ◽  
Author(s):  
Wei Lu ◽  
John A. Gray ◽  
Adam J. Granger ◽  
Matthew J. During ◽  
Roger A. Nicoll
Keyword(s):  
Nmda Receptors ◽  
Single Cell ◽  
Ampa Receptors ◽  
Substantial Evidence ◽  
Ampar Trafficking

Deletion of N-methyl-d-aspartate receptors (NMDARs) early in development results in an increase in the number of synaptic AMPA receptors (AMPARs), suggesting a role for NMDARs in negatively regulating AMPAR trafficking at developing synapses. Substantial evidence has shown that AMPAR subunits function differentially in AMPAR trafficking. However, the role of AMPAR subunits in the enhancement of AMPARs following NMDAR ablation remains unknown. We have now performed single-cell genetic deletions in double-floxed mice in which the deletion of GluN1 is combined with the deletion of GluA1 or GluA2. We find that the AMPAR enhancement following NMDAR deletion requires the GluA2 subunit, but not the GluA1 subunit, indicating a key role for GluA2 in the regulation of AMPAR trafficking in developing synapses.

Role of AMPA Receptor Desensitization and the Side Effects of a DMSO Vehicle on Reticulospinal EPSPs and Locomotor Activity

2005 ◽  
Vol 94 (6) ◽  
pp. 3951-3960 ◽  
Author(s):  
Nataliya A. Tsvyetlynska ◽  
Russell H. Hill ◽  
Sten Grillner
Keyword(s):  
Nmda Receptors ◽  
Ampa Receptor ◽  
Ampa Receptors ◽  
Pattern Generation ◽  
Network Activity ◽  
Excitatory Postsynaptic Potential ◽  
Receptor Desensitization ◽  
Neuronal Network Activity ◽  
The Brain

Activation of the vertebrate locomotor network is mediated by glutamatergic synaptic drive, normally initiated by the brain stem. Previous investigations have studied the role of glutamate receptors, especially NMDA receptors, in generating and regulating locomotor pattern generation. Few studies, however, have focused on the role of AMPA receptors in shaping network activity, especially with regard to their rapid desensitization. It is important to determine whether AMPA receptor desensitization plays a role in regulating neuronal network activity. We examined this question on both the network and synaptic levels in the lamprey ( Lampetra fluviatilis) spinal cord using a selective and potent inhibitor of AMPA receptor desensitization, cyclothiazide (CTZ). The solvent dimethyl sulfoxide (DMSO) is commonly used to dissolve this drug, as well as many others. Unexpectedly, the vehicle alone already at 0.02%, but not at 0.01%, caused significant increases in excitatory postsynaptic potential (EPSP) amplitudes and NMDA-induced locomotor frequency. The results indicate that DMSO may have a profound influence when used ≥0.02%, a concentration 10–50 times less than that most commonly used. Subsequently we applied CTZ concentrations ≤10 μM (DMSO ≤0.01%). CTZ (1.25–5 μM) caused an appreciable and significant increase in EPSPs mediated by non-NMDA receptors and in both AMPA- and NMDA-induced locomotor frequency, but no effects on EPSPs mediated by NMDA receptors. From the effects of CTZ it is apparent that AMPA receptor desensitization plays an important role in determining locomotor frequency and that this is likely a result of its limiting function on AMPA receptor–mediated EPSPs.

scholarly journals Possible Role of N-Methyl-D-Aspartate Receptors in Physiology and Pathophysiology of Cardiovascular System

2019 ◽  
Vol 20 (1) ◽  
pp. 3-13 ◽  
Author(s):  
Ivan Srejovic ◽  
Vladimir Jakovljevic ◽  
Vladimir Zivkovic ◽  
Dragan Djuric
Keyword(s):  
Nmda Receptors ◽  
Cardiovascular System ◽  
Ampa Receptors ◽  
Heart Function ◽  
Cell Types ◽  
Receptor Activation ◽  
Simultaneous Action ◽  
Cardiovascular Disorders ◽  
Voltage Dependent

Abstract N-methyl-D-aspartate (NMDA) receptors belong to ionotropic glutamate receptor family, together with α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, kainite receptors and δ-receptors. All of these receptors are tetramers composed of four subunits. NMDA receptors have several unique features in relation to other ionotropic glutamate receptors: requirement for simultaneous action of two coagonists, glutamate and glycine; dual control of receptor activation, ligand-dependent (by glutamate and glycine) and voltage-dependent (Mg2+ block) control; and influx of considerable amounts of Ca2+ following receptor activation. Increasing number of researches deals with physiological and pathophysiological roles of NMDA receptors outside of nerve tissues, especially in the cardiovascular system. NMDA receptors are found in all cell types represented in cardiovascular system, and their overstimulation in pathological conditions, such as hyperhomocysteinemia, is related to a range of cardiovascular disorders. On the other hand we demonstrated that blockade of NMDA receptors depresses heart function. There is a need for the intensive study of NMDA receptor in cardiovascular system as potential theraputical target both in prevention and treatment of cardiovascular disorders.

Role of non-NMDA receptors in vasopressin and oxytocin release from rat hypothalamo-neurohypophysial explants

2001 ◽  
Vol 280 (2) ◽  
pp. R313-R322 ◽  
Author(s):  
Delmore J. Morsette ◽  
Hanna Sidorowicz ◽  
Celia D. Sladek
Keyword(s):  
Nmda Receptors ◽  
Kainic Acid ◽  
Glutamate Receptor ◽  
Supraoptic Nucleus ◽  
Receptor Subtypes ◽  
Hormone Release ◽  
Oxytocin Release ◽  
Nmda Glutamate Receptor ◽  
Excitatory Transmitter

Glutamate is recognized as a prominent excitatory transmitter in the supraoptic nucleus (SON) and is involved in transmission of osmoregulatory information from the osmoreceptors to the vasopressin (VP) and oxytocin (OT) neurons. Explants of the hypothalamo-neurohypophysial system were utilized to characterize the roles of the non- N-methyl-d-aspartate (NMDA) glutamate receptor subtypes (non-NMDA-Rs), kainic acid receptors (KA-Rs), and aminopropionic acid receptors (AMPA-Rs) and to evaluate the interdependence of NMDA-Rs and non-NMDA-Rs in eliciting hormone release. Although both KA and AMPA increased hormone release, a specific agonist of the KA-Rs, SYM-2081, was not effective. This combined with the finding that cyclothiazide, an agent that inhibits the desensitization of AMPA-Rs, increased the VP response to both KA and AMPA indicates that the increase in hormone release induced by the non-NMDA agonists is mediated via AMPA-Rs, rather than KA-Rs. Inhibition of osmotically stimulated VP and OT release by a specific AMPA-R antagonist indicated that AMPA-Rs are essential for mediating osmotically stimulated hormone release. NMDA-stimulated VP but not OT release was prevented by blockade of non-NMDA-Rs, but AMPA-stimulated VP/OT release was not prevented by NMDA-R blockade.

AMPA Ionotropic Glutamate Receptors Pathogenesis Symptomatic Epilepsy in Gliomas of the Cerebral Hemispheres

10.12737/5909 ◽  
2014 ◽  
Vol 21 (3) ◽  
pp. 97-100
Author(s):  
Костюкевич ◽  
A. Kostyukevich ◽  
Очколяс ◽  
V. Ochkolyas ◽  
Скоромец ◽  
...  
Keyword(s):  
Ampa Receptors ◽  
Maximum Level ◽  
Epileptic Syndrome ◽  
Symptomatic Epilepsy ◽  
Glur1 Subunit ◽  
Growth Features ◽  
Morphological Research ◽  
Nr2a Subunit

The purpose of the research is to study the role of AMPA receptors of glutamate in the mechanisms of the development of epi-lepsy in the patients with gliomas of the big hemispheres of a brain. Materials and methods: 92 patients with gliomas of the big hemispheres of a brain have been examined. Immune enzyme method of semi-quantitative determination of the level of auto-antibodies to NR2A subunit of NMDA and GluR1 subunit of AMPA receptors of glutamate was used. Results: The frequency and clinical features of symptomatic epilepsy have been studied. The reaction of NMDA and of AMPA receptors of glutamate depending on localization and degree of malignance and features of clinical course of the disease, have been examined. Conclusion: A high-technology of patho-morphological research of brain tumors made in recent years has revealed that glial tumors start releasing glutamate by themselves, as their anaplasia level increases, which causes exitotoxical effect in anatomical lines of peritumoral area. Such blastomastoma growth features form specificity of clinical aspect of disease, including epileptic syndrome. It is shown dominative increase the level of auto-antibodies to GluR1 subunit of AMPA receptors of glutamate in the patients with gliomas, current with epileptic syndrome. Under the effect of the tumor on the frontal and temporal share the maximum level of autoantibodies, mainly to GluR1 subunit of AMPA receptors of glutamate is registered.

Role of small nuclear RNAs in eukaryotic gene expression

2013 ◽  
Vol 54 ◽  
pp. 79-90 ◽  
Author(s):  
Saba Valadkhan ◽  
Lalith S. Gunawardane
Keyword(s):  
Gene Expression ◽  
Protein Interactions ◽  
Rna Stability ◽  
Splice Sites ◽  
Branch Site ◽  
Small Nuclear Rnas ◽  
Eukaryotic Gene Expression ◽  
Eukaryotic Gene ◽  
Rna Biogenesis

Eukaryotic cells contain small, highly abundant, nuclear-localized non-coding RNAs [snRNAs (small nuclear RNAs)] which play important roles in splicing of introns from primary genomic transcripts. Through a combination of RNA–RNA and RNA–protein interactions, two of the snRNPs, U1 and U2, recognize the splice sites and the branch site of introns. A complex remodelling of RNA–RNA and protein-based interactions follows, resulting in the assembly of catalytically competent spliceosomes, in which the snRNAs and their bound proteins play central roles. This process involves formation of extensive base-pairing interactions between U2 and U6, U6 and the 5′ splice site, and U5 and the exonic sequences immediately adjacent to the 5′ and 3′ splice sites. Thus RNA–RNA interactions involving U2, U5 and U6 help position the reacting groups of the first and second steps of splicing. In addition, U6 is also thought to participate in formation of the spliceosomal active site. Furthermore, emerging evidence suggests additional roles for snRNAs in regulation of various aspects of RNA biogenesis, from transcription to polyadenylation and RNA stability. These snRNP-mediated regulatory roles probably serve to ensure the co-ordination of the different processes involved in biogenesis of RNAs and point to the central importance of snRNAs in eukaryotic gene expression.

Cell-specific regulation of IRS-1 gene expression: role of E box and C/EBP binding site in HepG2 cells and CHO cells

Diabetes ◽  
1997 ◽  
Vol 46 (3) ◽  
pp. 354-362 ◽  
Author(s):  
K. Matsuda ◽  
E. Araki ◽  
R. Yoshimura ◽  
K. Tsuruzoe ◽  
N. Furukawa ◽  
...  
Keyword(s):  
Gene Expression ◽  
Binding Site ◽  
Cho Cells ◽  
Hepg2 Cells ◽  
E Box ◽  
Specific Regulation
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