JN Watch the video to see how APS reaches out to developing nations.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

J Neurophysiol (June 16, 2004). doi:10.1152/jn.00466.2004
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
92/4/2610    most recent
00466.2004v2
00466.2004v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (7)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Faria, L. C.
Right arrow Articles by Mody, I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Faria, L. C.
Right arrow Articles by Mody, I.
Submitted on May 5, 2004
Accepted on June 9, 2004

Protective Effect of Ifenprodil against Spreading Depression in the Mouse Entorhinal Cortex

Leonardo C. Faria1 and Istvan Mody2*

1 Neurologia e Neurocirurgia, Universidade Federal de Sao Paulo - UNIFESP, Sao Paulo, SP, Brazil; Neurology and Physiology, University of California at Los Angeles - UCLA, Los Angeles, California, USA
2 Neurology and Physiology, University of California at Los Angeles - UCLA, Los Angeles, California, USA

* To whom correspondence should be addressed. E-mail: mody{at}ucla.edu.

In the brain, spreading depression (SD) is characterized by a large extracellular DC shift, a massive failure of ion homeostasis and a transient cessation of neuronal function. Clinically, SD is believed to be involved in various neurological disorders including migraine and cerebrovascular diseases. The propagation of cortical SD requires the release of glutamate, and NMDA receptors play a crucial role in this process. Here, we have isolated the NMDA-receptor-mediated component of extracellularly recorded field EPSPs (fEPSPs) in layers 2-3 of the entorhinal cortex of murine brain slices. In the absence of GABAA and AMPA receptor mediated synaptic transmission, stimulation of layer 6 afferents every 15 - 90 s elicited spontaneous SD on average within 18.5 min after the start of the stimulation. In the presence of ifenprodil, an NR2B receptor subunit-selective NMDA receptor antagonist, the occurrence of SD was nearly abolished. Our results are consistent with an important role of NR2B subunits in triggering SD in the entorhinal cortex.




This article has been cited by other articles:


Home page
 J. Pharmacol. Exp. Ther.Home page
M. Peeters, M. J. Gunthorpe, P. J. L. M. Strijbos, P. Goldsmith, N. Upton, and M. F. James
Effects of Pan- and Subtype-Selective N-Methyl-D-aspartate Receptor Antagonists on Cortical Spreading Depression in the Rat: Therapeutic Potential for Migraine
J. Pharmacol. Exp. Ther., May 1, 2007; 321(2): 564 - 572.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 2004 by the The American Physiological Society.