Localization of glutamate receptors in developing cortical neurons in culture and relationship to susceptibility to excitotoxicity

2006 ◽  
Vol 498 (2) ◽  
pp. 277-294 ◽  
Author(s):  
A.E. King ◽  
R.S. Chung ◽  
J.C. Vickers ◽  
T.C. Dickson
Keyword(s):  
Glutamate Receptors ◽  
Cortical Neurons

Glutamate receptors in cortical plasticity: molecular and cellular biology

1997 ◽  
Vol 77 (1) ◽  
pp. 217-255 ◽  
Author(s):  
L. Kaczmarek ◽  
M. Kossut ◽  
J. Skangiel-Kramska
Keyword(s):  
Glutamate Receptors ◽  
Cortical Neurons ◽  
Cortical Plasticity ◽  
Excitatory Input ◽  
Cellular Biology ◽  
Metabotropic Receptors ◽  
Functional Studies ◽  
Neuron Response ◽  
Plastic Changes ◽  
Protein Immunoreactivity

Glutamate receptors (GluRs) provide the major excitatory input to cortical neurons. Four main subtypes of GluRs are distinguished, namely, N-methyl-D-aspartate, alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid, kainate, and metabotropic receptors. All of them have been implicated in neuronal plasticity, and this paper reviews data that may be pertinent to the role played by GluRs in neocortical plasticity both in adult animals as well as during postnatal development. Emphasis is given to receptor distribution analyzed by various means, such as physiological responses, ligand binding as revealed by receptor autoradiography, and expression of receptor subunits at both mRNA and protein (immunoreactivity) levels. Possible mechanisms of involvement of GluRs in plastic changes on cortical neuron response are reviewed, and data on up- and downregulation of GluRs in neocortical plasticity are summarized. Functional studies involving either activation or blocking, and effects of such manipulation on cortical plasticity are discussed.

Propofol Inhibits Phosphorylation of N -methyl-d-aspartate Receptor NR1 Subunits in Neurons

2006 ◽  
Vol 104 (4) ◽  
pp. 763-769 ◽  
Author(s):  
Seth Kingston ◽  
Limin Mao ◽  
Lu Yang ◽  
Anish Arora ◽  
Eugene E. Fibuch ◽  
...  
Keyword(s):  
Glutamate Receptors ◽  
Okadaic Acid ◽  
Protein Phosphatase ◽  
Cortical Neurons ◽  
Protein Phosphatase 2A ◽  
Ionotropic Glutamate Receptors ◽  
Dependent Manner ◽  
Calyculin A ◽  
General Anesthetic ◽  
Phosphatase 2A

Background Anesthetics may interact with ionotropic glutamate receptors to produce some of their biologic actions. Cellular studies reveal that the ionotropic glutamate receptors, N-methyl-D-aspartate receptors (NMDARs), can be phosphorylated on their NR1 subunits at the C-terminal serine residues, which is a major mechanism for the regulation of NMDAR functions. It is currently unknown whether anesthetics have any modulatory effects on NMDAR NR1 subunit phosphorylation. Methods The possible effect of a general anesthetic propofol on phosphorylation of NR1 subunits at serine 897 (pNR1S897) and 896 (pNR1S896) was detected in cultured rat cortical neurons. Results Propofol consistently reduced basal levels of pNR1S897 and pNR1S896 in a concentration-dependent manner. This reduction was rapid as the reliable reduction of pNR1S896 developed 1 min after propofol administration. Pretreatment of cultures with the protein phosphatase 2A inhibitors okadaic acid or calyculin A blocked the effect of propofol on the NR1 phosphorylation, whereas okadaic acid or calyculin A alone did not alter basal pNR1S897 and pNR1S896 levels. In addition, propofol decreased tyrosine phosphorylation of protein phosphatase 2A at tyrosine 307, resulting in an increase in protein phosphatase 2A activity. In the presence of propofol, the NMDAR agonist-induced intracellular Ca2+ increase was impaired in neurons with dephosphorylated NR1 subunits. Conclusions Together, these data indicate an inhibitory effect of a general anesthetic propofol on NMDAR NR1 subunit phosphorylation in neurons. This inhibition was mediated through a signaling mechanism involving activation of protein phosphatase 2A.

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 The Marine Guanidine Alkaloid Crambescidin 816 Induces Calcium Influx and Cytotoxicity in Primary Cultures of Cortical Neurons through Glutamate Receptors

2017 ◽  
Vol 8 (7) ◽  
pp. 1609-1617 ◽  
Author(s):  
Aida G. Mendez ◽  
Andrea Boente Juncal ◽  
Siguara B. L. Silva ◽  
Olivier P. Thomas ◽  
Víctor Martín Vázquez ◽  
...  
Keyword(s):  
Glutamate Receptors ◽  
Cortical Neurons ◽  
Calcium Influx ◽  
Primary Cultures

Estrogen Receptors and Type 1 Metabotropic Glutamate Receptors Are Interdependent in Protecting Cortical Neurons against β-Amyloid Toxicity

2011 ◽  
Vol 81 (1) ◽  
pp. 12-20 ◽  
Author(s):  
Simona Federica Spampinato ◽  
Gemma Molinaro ◽  
Sara Merlo ◽  
Luisa Iacovelli ◽  
Filippo Caraci ◽  
...  
Keyword(s):  
Estrogen Receptors ◽  
Glutamate Receptors ◽  
Cortical Neurons ◽  
Metabotropic Glutamate Receptors ◽  
Metabotropic Glutamate ◽  
Amyloid Toxicity ◽  
Β Amyloid
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