scholarly journals Erratum: Corrigendum: AMPA receptor-mediated regulation of a Gi-protein in cortical neurons

Nature ◽  
2017 ◽  
Vol 554 (7692) ◽  
pp. 392-392
Author(s):  
Yizheng Wang ◽  
Daniel L. Small ◽  
Danica B. Stanimirovic ◽  
Paul Morley ◽  
Jon P. Durkin
Keyword(s):  
Ampa Receptor ◽  
Cortical Neurons ◽  
Gi Protein

AMPA receptor-mediated regulation of a Gi-protein in cortical neurons

Nature ◽  
10.1038/39062 ◽  
1997 ◽  
Vol 389 (6650) ◽  
pp. 502-504 ◽  
Author(s):  
Yizheng Wang ◽  
Daniel L. Small ◽  
Danica B. Stanimirovic ◽  
Paul Morley ◽  
Jon P. Durkin
Keyword(s):  
Ampa Receptor ◽  
Cortical Neurons ◽  
Gi Protein

LY392098, a novel AMPA receptor potentiator: electrophysiological studies in prefrontal cortical neurons

2001 ◽  
Vol 40 (8) ◽  
pp. 992-1002 ◽  
Author(s):  
Polly Baumbarger ◽  
Mark Muhlhauser ◽  
Charles R Yang ◽  
Eric S Nisenbaum
Keyword(s):  
Ampa Receptor ◽  
Cortical Neurons ◽  
Prefrontal Cortical ◽  
Electrophysiological Studies

scholarly journals Yy1 regulates Senp1 contributing to AMPA receptor GluR1 expression following neuronal depolarization

2019 ◽  
Vol 26 (1) ◽  
Author(s):  
Tao Wu ◽  
Mary E. Donohoe
Keyword(s):  
Gene Expression ◽  
Ampa Receptor ◽  
Neuronal Activity ◽  
Cortical Neurons ◽  
Expression Patterns ◽  
Luciferase Assay ◽  
Regulation Mechanism ◽  
Phosphatase Inhibitors ◽  
Ampa Receptor Subunit

Abstract Background Neuronal activity-induced changes in gene expression patterns are important mediators of neuronal plasticity. Many neuronal genes can be activated or inactivated in response to neuronal depolarization. Mechanisms that activate gene transcription are well established, but activity-dependent mechanisms that silence transcription are less understood. It is also not clear what is the significance of inhibiting these genes during neuronal activity. Methods Quantitative Real Time-PCR, western blot and immunofluorescence staining were performed to examine the expression of Senp1 and GluR1 in mouse cortical neurons. The alterations of Yy1 phosphorylation upon neuronal depolarization and the interaction of Yy1 with Brd4 were studied by protein co-immunoprecipitation. The regulators of Yy1 phosphorylation were identified by phosphatase inhibitors. Chromatin immunoprecipitation, in vitro DNA binding assay, luciferase assay and gene knockdown experiments were used to validate the roles of Yy1 and its phosphorylation as well as Brd4 in regulating Senp1 expression. Results We report that neuronal depolarization deactivates the transcription of the SUMO protease Senp1, an important component regulating synaptic transmission, scaling, and plasticity, through Yy1. In un-stimulated neurons, Senp1 transcription is activated by a Yy1-Brd4 transcription factor protein complex assembled on the Senp1 promoter. Upon membrane depolarization, however, Yy1 is dephosphorylated and the Yy1-Brd4 complex is evicted from the Senp1 promoter, reducing Senp1 transcription levels. Both Yy1 and Senp1 promote the expression of AMPA receptor subunit GluR1, a pivotal component in learning and memory. Conclusions These results reveal an axis of Yy1/Brd4-Senp1 which regulates the expression of GluR1 during neuronal depolarization. This implicates a regulation mechanism in silencing gene expression upon neuronal activity.

scholarly journals Roles of 5-HT 1A receptor in the expression of AMPA receptor and BDNF in developing mouse cortical neurons

2017 ◽  
Vol 115 ◽  
pp. 13-20 ◽  
Author(s):  
Yuko Yoshimura ◽  
Chihiro Ishikawa ◽  
Haruki Kasegai ◽  
Tomoyuki Masuda ◽  
Masaaki Yoshikawa ◽  
...  
Keyword(s):  
Ampa Receptor ◽  
Cortical Neurons

scholarly journals Evidence that Functional Glutamate Receptors are not Expressed on Rat or Human Cerebromicrovascular Endothelial Cells

1998 ◽  
Vol 18 (4) ◽  
pp. 396-406 ◽  
Author(s):  
Paul Morley ◽  
Daniel L. Small ◽  
Christine L. Murray ◽  
Geoffrey A. Mealing ◽  
Michael O. Poulter ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Nmda Receptor ◽  
Glutamate Receptors ◽  
Glutamate Receptor ◽  
Ampa Receptor ◽  
Cortical Neurons ◽  
Cerebral Vessels ◽  
Rt Pcr ◽  
Metabotropic Glutamate ◽  
Rat Cortical Neurons

Excitatory amino acids can modify the tone of cerebral vessels and permeability of the blood-brain barrier (BBB) by acting directly on endothelial cells of cerebral vessels or indirectly by activating receptors expressed on other brain cells. In this study we examined whether rat or human cerebromicrovascular endothelial cells (CEC) express ionotropic and metabotropic glutamate receptors. Glutamate and the glutamate receptor agonists N-methyl-d-aspartate (NMDA), α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA), and kainate failed to increase [Ca2+]i in either rat or human microvascular and capillary CEC but elicited robust responses in primary rat cortical neurons, as measured by fura-2 fluorescence. The absence of NMDA and AMPA receptors in rat and human CEC was further confirmed by the lack of immunocytochemical staining of cells by antibodies specific for the AMPA receptor subunits GluR1, GluR2/3, and GluR4 and the NMDA receptor subunits NR1, NR2A, and NR2B. We failed to detect mRNA expression of the AMPA receptor subunits GluR1 to GluR4 or the NMDA receptor subunits NR11XX, NR10XX, and NR2A to NR2C in both freshly isolated rat and human microvessels and cultured CEC using reverse transcriptase polymerase chain reaction (RT-PCR). Cultured rat CEC expressed mRNA for KA1 or KA2 and GluR5 subunits. Primary rat cortical neurons were found to express GluR1 to GluR3 and NR1, NR2A, and NR2B by both immunocytochemistry and RT-PCR and KA1, KA2, GluR5, GluR6, and GluR7 by RT-PCR. Moreover, the metabotropic glutamate receptor agonist 1-amino-cyclopentyl-1 S, 3 R-dicorboxylate (1 S,3 R-trans-ACPD), while eliciting both inositol trisphosphate and [Ca2+]i increases and inhibiting forskolin-stimulated cyclic AMP in cortical neurons, was unable to induce either of these responses in rat or human CEC. These results strongly suggest that both rat and human CEC do not express functional glutamate receptors. Therefore, excitatory amino acid-induced changes in the cerebral microvascular tone and BBB permeability must be affected indirectly, most likely by mediators released from the adjacent glutamate-responsive cells.

scholarly journals NMDA Receptor Activation by Spontaneous Glutamatergic Neurotransmission

2009 ◽  
Vol 101 (5) ◽  
pp. 2290-2296 ◽  
Author(s):  
Felipe Espinosa ◽  
Ege T. Kavalali
Keyword(s):  
Nmda Receptor ◽  
Nmda Receptors ◽  
Ampa Receptor ◽  
Cortical Neurons ◽  
Glutamate Release ◽  
Receptor Activation ◽  
Receptor Activity ◽  
Resting Membrane Potential ◽  
Nmda Current ◽  
Nmda Receptor Activation

Under physiological conditions N-methyl-d-aspartate (NMDA) receptor activation requires coincidence of presynaptic glutamate release and postsynaptic depolarization due to the voltage-dependent block of these receptors by extracellular Mg2+. Therefore spontaneous neurotransmission in the absence of action potential firing is not expected to lead to significant NMDA receptor activation. Here we tested this assumption in layer IV neurons in neocortex at their resting membrane potential (approximately −67 mV). In long-duration stable recordings, we averaged a large number of miniature excitatory postsynaptic currents (mEPSCs, >100) before or after application of dl-2 amino 5-phosphonovaleric acid, a specific blocker of NMDA receptors. The difference between the two mEPSC waveforms showed that the NMDA current component comprises ∼20% of the charge transfer during an average mEPSC detected at rest. Importantly, the contribution of the NMDA component was markedly enhanced at membrane potentials expected for the depolarized up states (approximately −50 mV) that cortical neurons show during slow oscillations in vivo. In addition, partial block of the α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor component of the mEPSCs did not cause a significant reduction in the NMDA component, indicating that potential AMPA receptor-driven local depolarizations did not drive NMDA receptor activity at rest. Collectively these results indicate that NMDA receptors significantly contribute to signaling at rest in the absence of dendritic depolarizations or concomitant AMPA receptor activity.

scholarly journals Effects of sodium arsenite on neurite outgrowth and glutamate AMPA receptor expression in mouse cortical neurons

2013 ◽  
Vol 37 ◽  
pp. 197-206 ◽  
Author(s):  
Fumihiko Maekawa ◽  
Takashi Tsuboi ◽  
Manami Oya ◽  
Kyaw Htet Aung ◽  
Shinji Tsukahara ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Ampa Receptor ◽  
Cortical Neurons ◽  
Sodium Arsenite ◽  
Receptor Expression

Mechanism of inhibition by ethanol of NMDA and AMPA receptor channel functions in cultured rat cortical neurons

2000 ◽  
Vol 362 (6) ◽  
pp. 568-576 ◽  
Author(s):  
Not Available Not Available ◽  
Not Available Not Available ◽  
Not Available Not Available ◽  
Not Available Not Available ◽  
Not Available Not Available
Keyword(s):  
Ampa Receptor ◽  
Cortical Neurons ◽  
Mechanism Of Inhibition ◽  
Rat Cortical Neurons ◽  
Receptor Channel
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