Regional release of [3H] adenosine derivatives from rat brain in vivo: effect of excitatory amino acids, opiate agonists, and benzodiazepines

1980 ◽  
Vol 58 (11) ◽  
pp. 1262-1278 ◽  
Author(s):  
K. Jhamandas ◽  
A. Dumbrille
PLoS ONE ◽  
2008 ◽  
Vol 3 (10) ◽  
pp. e3543 ◽  
Author(s):  
Renée E. Haskew-Layton ◽  
Alena Rudkouskaya ◽  
Yiqiang Jin ◽  
Paul J. Feustel ◽  
Harold K. Kimelberg ◽  
...  

1984 ◽  
Vol 9 (3) ◽  
pp. 367-385 ◽  
Author(s):  
M. K. Gaitonde ◽  
Margaret D. James ◽  
Gwyneth M. Evans
Keyword(s):  

Synapse ◽  
1992 ◽  
Vol 12 (4) ◽  
pp. 271-280 ◽  
Author(s):  
Petrus J. Pauwels ◽  
Harrie P. Van Assouw ◽  
Luc Peeters ◽  
Marc Moeremans ◽  
Jos�e E. Leysen

1991 ◽  
Vol 69 (7) ◽  
pp. 1123-1128 ◽  
Author(s):  
David Lodge ◽  
Martyn G. Jones ◽  
Andrew J. Palmer

Although the N-methyl-D-aspartate (NMDA) subtype of L-glutamate receptor is well characterized, the significance of non-NMDA glutamate-sensitive binding sites is not well documented. In this study, a new tricyclic quinoxalinedione (NBQX) and an arthropod toxin (philanthotoxin) were shown to block responses of spinal neurones in vivo to kainate, quisqualate, and AMPA in parallel but had little effect on responses to NMDA. Philanthotoxin appeared to be a use-dependent antagonist consistent with a channel-blocking mode of action. On cortical wedges in vitro, however, NBQX proved to be a more potent antagonist of AMPA and quisqualate than of kainate (pA2 values of 7.1, 7.0, and 5.6, respectively) with no effect at 10 μM on responses to NMDA. These studies provide evidence that on cortical neurones, but not on spinal neurones, AMPA and kainate depolarize by pharmacologically different mechanisms.Key words: glutamate receptors, quinoxalinediones, philanthotoxin, AMPA, kainate.


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