Distinct NMDA and AMPA Receptor–Mediated Responses in Mouse and Human Cajal-Retzius Cells

2001 ◽  
Vol 86 (5) ◽  
pp. 2642-2646 ◽  
Author(s):  
Shao-Ming Lu ◽  
Nada Zecevic ◽  
Hermes H. Yeh
Keyword(s):  
Nmda Receptor ◽  
Glutamate Receptor ◽  
Differential Sensitivity ◽  
Voltage Dependent ◽  
Cell Current ◽  
Nmda Glutamate Receptor ◽  
Retzius Cells ◽  
Glutamate Receptor Agonist ◽  
Human And Mouse ◽  
Cortical Slices

This study examined glutamate-activated current responses of mouse and human Cajal-Retzius (C-R) cells. Thin cortical slices were prepared from the brains of mice 4–6 days after birth and from those of midgestational human fetuses. Both human and mouse C-R cells displayed glutamate-induced whole-cell current responses that were voltage-dependent and included an N-methyl-d-aspartate (NMDA) receptor–mediated component that was differentially sensitive to blockade by the NMDA receptor antagonists 2-amino-5-phosphonovaleric acid and ifenprodil. α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), a non-NMDA glutamate receptor agonist, induced current responses in human but not in mouse C-R cells. These results, taken together, lead us to conclude that human C-R cells express both NMDA and AMPA types of glutamate receptors very early during development of the cortex. In contrast, mouse C-R cells express only the NMDA type of glutamate receptor. Thus we demonstrate a species-dependent sensitivity of C-R cells to glutamate and postulate that this differential sensitivity may account in part for a species-dependent difference in the persistence of C-R cells during cortical development.

Metabotropic glutamate receptor agonist DCG-IV as NMDA receptor agonist in immature rat hippocampal neurons

1994 ◽  
Vol 262 (3) ◽  
pp. 287-291 ◽  
Author(s):  
Volker W. Wilsch ◽  
Vladimir I. Pidoplichko ◽  
Thoralf Opitz ◽  
Haruhiko Shinozaki ◽  
Klaus G. Reymann
Keyword(s):  
Nmda Receptor ◽  
Glutamate Receptor ◽  
Hippocampal Neurons ◽  
Receptor Agonist ◽  
Metabotropic Glutamate Receptor ◽  
Immature Rat ◽  
Metabotropic Glutamate ◽  
Glutamate Receptor Agonist

Xenon Acts by Inhibition of Non–N -methyl-d-aspartate Receptor–mediated Glutamatergic Neurotransmission in Caenorhabditis elegans 

2005 ◽  
Vol 103 (3) ◽  
pp. 508-513 ◽  
Author(s):  
Peter Nagele ◽  
Laura B. Metz ◽  
C Michael Crowder
Keyword(s):  
Nitrous Oxide ◽  
Caenorhabditis Elegans ◽  
Nmda Receptor ◽  
Glutamate Receptor ◽  
Glutamatergic Transmission ◽  
Wild Type ◽  
C Elegans ◽  
Aspartate Receptor ◽  
Nmda Glutamate Receptor ◽  
Response Transformation

Background Electrophysiologic experiments in rodents have found that nitrous oxide and xenon inhibit N-methyl-D-aspartate (NMDA)-type glutamate receptors. These findings led to the hypothesis that xenon and nitrous oxide along with ketamine form a class of anesthetics with the identical mechanism, NMDA receptor antagonism. Here, the authors ask in Caenorhabditis elegans whether xenon, like nitrous oxide, acts by a NMDA receptor-mediated mechanism. Methods Xenon:oxygen mixtures were delivered into sealed chambers until the desired concentration was achieved. The effects of xenon on various behaviors were measured on wild-type and mutant C. elegans strains. Results With an EC50 of 15-20 vol% depending on behavioral endpoint, xenon altered C. elegans locomotion in a manner indistinguishable from that of mutants in glutamatergic transmission. Xenon reduced the frequency and duration of backward locomotion without altering its speed or other behaviors tested. Mutation of glr-1, encoding a non-NMDA glutamate receptor subunit, abolished the behavioral effects of xenon; however, mutation of nmr-1, which encodes the pore-forming subunit of an NMDA glutamate receptor previously shown to be required for nitrous oxide action, did not significantly alter xenon response. Transformation of the glr-1 mutant with the wild-type glr-1 gene partially restored xenon sensitivity, confirming that glr-1 was necessary for the full action of xenon. Conclusions Xenon acts in C. elegans to alter locomotion through a mechanism requiring the non-NMDA glutamate receptor encoded by glr-1. Unlike for the action of nitrous oxide in C. elegans, the NMDA receptor encoded by nmr-1 is not essential for sensitivity to xenon.

scholarly journals N-Methyl-D-aspartate Glutamate Receptor Modulates Cardiovascular and Neuroendocrine Responses Evoked by Hemorrhagic Shock in Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Cristiane Busnardo ◽  
Aline Fassini ◽  
Bruno Rodrigues ◽  
José Antunes-Rodrigues ◽  
Carlos C. Crestani ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Hemorrhagic Shock ◽  
Glutamate Receptor ◽  
Recovery Period ◽  
Intraperitoneal Administration ◽  
Receptor Activation ◽  
Vasopressin Release ◽  
Bed Nucleus ◽  
Nmda Glutamate Receptor ◽  
The Brain

Here, we report the participation of N-methyl-D-aspartate (NMDA) glutamate receptor in the mediation of cardiovascular and circulating vasopressin responses evoked by a hemorrhagic stimulus. In addition, once NMDA receptor activation is a prominent mechanism involved in nitric oxide (NO) synthesis in the brain, we investigated whether control of hemorrhagic shock by NMDA glutamate receptor was followed by changes in NO synthesis in brain supramedullary structures involved in cardiovascular and neuroendocrine control. Thus, we observed that intraperitoneal administration of the selective NMDA glutamate receptor antagonist dizocilpine maleate (MK801, 0.3 mg/kg) delayed and reduced the magnitude of hemorrhage-induced hypotension. Besides, hemorrhage induced a tachycardia response in the posthemorrhage period (i.e., recovery period) in control animals, and systemic treatment with MK801 caused a bradycardia response during hemorrhagic shock. Hemorrhagic stimulus increased plasma vasopressin levels during the recovery period and NMDA receptor antagonism increased concentration of this hormone during both the hemorrhage and postbleeding periods in relation to control animals. Moreover, hemorrhagic shock caused a decrease in NOx levels in the paraventricular nucleus of the hypothalamus (PVN), amygdala, bed nucleus of the stria terminalis (BNST), and ventral periaqueductal gray matter (vPAG). Nevertheless, treatment with MK801 did not affect these effects. Taken together, these results indicate that the NMDA glutamate receptor is involved in the hemorrhagic shock by inhibiting circulating vasopressin release. Our data also suggest a role of the NMDA receptor in tachycardia, but not in the decreased NO synthesis in the brain evoked by hemorrhage.

NMDA-Receptor-Dependent Synaptic Activation of Voltage-Dependent Calcium Channels in Basolateral Amygdala

2000 ◽  
Vol 83 (2) ◽  
pp. 685-692 ◽  
Author(s):  
Jeffrey L. Calton ◽  
Maeng-Hee Kang ◽  
Wilkie A. Wilson ◽  
Scott D. Moore
Keyword(s):  
Nmda Receptor ◽  
Calcium Channels ◽  
Basolateral Amygdala ◽  
Pyramidal Cells ◽  
Activation Threshold ◽  
Afferent Stimulus ◽  
Voltage Dependent ◽  
Nmda Glutamate Receptors ◽  
Voltage Dependent Calcium Channels ◽  
Cell Current

Afferent stimulation of pyramidal cells in the basolateral amygdala produced mixed excitatory postsynaptic potentials (EPSPs) mediated by N-methyl-d-aspartate (NMDA) and non-NMDA glutamate receptors during whole cell current-clamp recordings. In the presence of GABAA receptor blockade, the mixed EPSPs recruited a large “all-or-none” depolarizing event. This recruited event was voltage dependent and had a distinct activation threshold. An analogous phenomenon elicited by exogenous glutamate in the presence of tetrodotoxin (TTX) was blocked by Cd2+, suggesting that the event was a Ca2+ spike. Selective glutamatergic blockade revealed that these Ca2+ spikes were recruited readily by single afferent stimulus pulses that elicited NMDA EPSPs. In contrast, non-NMDA EPSPs induced by single stimuli failed to elicit the Ca2+ spike even at maximal stimulus intensities although these non-NMDA EPSPs depolarized the soma more effectively than mixed EPSPs. Elongation of non-NMDA EPSPs by cyclothiazide or brief trains of stimulation were also unable to elicit the Ca2+ spike. Blockade of K+ channels with intracellular Cs+enabled single non-NMDA EPSPs to activate the Ca2+ spike. The finding that voltage-dependent calcium channels are activated preferentially by NMDA-receptor-mediated EPSPs provides a mechanism for NMDA-receptor-dependent plasticity independent of Ca2+influx through the NMDA receptor.

Potentiation of mossy fiber-evoked EPSPs in turtle cerebellar Purkinje cells by the metabotropic glutamate receptor agonist 1S,3R-ACPD

1992 ◽  
Vol 67 (4) ◽  
pp. 1006-1008 ◽  
Author(s):  
G. A. Kinney ◽  
N. T. Slater
Keyword(s):  
Nmda Receptor ◽  
Purkinje Cells ◽  
Glutamate Receptor ◽  
Metabotropic Glutamate Receptor ◽  
Mossy Fiber ◽  
Mossy Fibers ◽  
Nmda Receptor Antagonist ◽  
Metabotropic Glutamate ◽  
Cerebellar Purkinje Cells ◽  
Glutamate Receptor Agonist

1. The effects of the metabotropic glutamate receptor (mGluR) agonist 1S,3R-ACPD on excitatory postsynaptic potentials (EPSPs) evoked by stimulation of mossy fibers (MF) and parallel fibers (PF) were examined in turtle cerebellar Purkinje cells. 2. 1S,3R-ACPD (1-25 microM) reversibly potentiated the amplitude of the MF-evoked EPSPs and revealed a late, slow EPSP component, but was without effect on PF-evoked EPSPs. The potentiation of both components of MF-evoked EPSPs was dose dependent, with an ED50 of approximately 3 microM. At higher doses (15-25 microM) 1S,3R-ACPD produced a direct depolarization of Purkinje cells in 57% of cells examined. 3. The enhancement of MF EPSPs by 1S,3R-ACPD was blocked by the N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-5-phosphonovalerate (AP-5), but not by the mGluR antagonist L-2-amino-3-phosphonopionic acid (L-AP3; 1 mM), or the 1R,3S isomer of ACPD (25-500 microM). 4. The results demonstrate that mGluR activation by 1S,3R-ACPD produces a potent, stereospecific facilitation of NMDA receptor-mediated transmission at the MF-granule cell synapse.

In vivo evaluation of [11C]CNS-5161 as a use-dependent ligand for the NMDA glutamate receptor channel

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S595-S595 ◽  
Author(s):  
Wynne K Schiffer ◽  
Deborah Pareto-Onghena ◽  
HaiTao Wu ◽  
Kuo-Shyan Lin ◽  
Andrew R Gibbs ◽  
...  
Keyword(s):  
Glutamate Receptor ◽  
In Vivo Evaluation ◽  
Nmda Glutamate Receptor ◽  
Receptor Channel
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