NMDA receptor activation induces glutamate release through nitric oxide synthesis in guinea pig dentate gyrus

1996 ◽  
Vol 728 (1) ◽  
pp. 105-110 ◽  
Author(s):  
Koji Nei ◽  
Shogo Matsuyama ◽  
Hisato Shuntoh ◽  
Chikako Tanaka
Keyword(s):  
Nitric Oxide ◽  
Nmda Receptor ◽  
Guinea Pig ◽  
Dentate Gyrus ◽  
Glutamate Release ◽  
Receptor Activation ◽  
Nitric Oxide Synthesis ◽  
Nmda Receptor Activation

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.

Icilin induces a hyperthermia in rats that is dependent on nitric oxide production and NMDA receptor activation

2008 ◽  
Vol 578 (2-3) ◽  
pp. 201-208 ◽  
Author(s):  
Zhe Ding ◽  
Teresa Gomez ◽  
Jennifer L. Werkheiser ◽  
Alan Cowan ◽  
Scott M. Rawls
Keyword(s):  
Nitric Oxide ◽  
Nmda Receptor ◽  
Receptor Activation ◽  
Nitric Oxide Production ◽  
Oxide Production ◽  
Nmda Receptor Activation

scholarly journals Glutamate release via NO production evoked by NMDA in the NTS enhances hypotension and bradycardia in vivo

2001 ◽  
Vol 280 (5) ◽  
pp. R1285-R1291 ◽  
Author(s):  
Isamu Matsuo ◽  
Yoshitaka Hirooka ◽  
Kiyoshi Hironaga ◽  
Kenichi Eshima ◽  
Hideaki Shigematsu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Sympathetic Nerve Activity ◽  
Glutamate Release ◽  
Cardiovascular Responses ◽  
Receptor Activation ◽  
In Vivo Microdialysis ◽  
No Production ◽  
Nerve Activity ◽  
Nmda Receptor Activation

Nitric oxide (NO) in the nucleus tractus solitarii (NTS) plays an important role in regulating sympathetic nerve activity. The aims of this study were to determine whether the activation of N-methyl-d-aspartate (NMDA) receptors in the NTS facilitates the release ofl-glutamate (Glu) via NO production, and, if so, to determine whether this mechanism is involved in the depressor and bradycardic responses evoked by NMDA. We measured the production of NO in the NTS as NO[Formula: see text] and NO[Formula: see text](NOx) or Glu levels by in vivo microdialysis before, during, and after infusion of NMDA in anesthetized rats. We also examined effects of N ω-nitro-l-arginine methyl ester (l-NAME) on the changes in these levels. NMDA elicited depressor and bradycardic responses and increased the levels of NOx and Glu. l-NAME abolished the increases in the levels of NOx and Glu and attenuated cardiovascular responses evoked by NMDA. These results suggest that NMDA receptor activation in the NTS induces Glu release through NO synthesis and that Glu released via NO enhances depressor and bradycardic responses.

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