JN Information on EB 2010
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

J Neurophysiol (June 28, 2006). doi:10.1152/jn.00280.2006
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
96/4/1829    most recent
00280.2006v1
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 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 Google Scholar
Google Scholar
Right arrow Articles by Negrete-Diaz, J. V.
Right arrow Articles by Rodriguez-Moreno, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Negrete-Diaz, J. V.
Right arrow Articles by Rodriguez-Moreno, A.
Submitted on March 15, 2006
Accepted on June 6, 2006

Kainate receptor-mediated inhibition of glutamate release involves protein kinase A in the mouse hippocampus

Jose Vicente Negrete-Diaz1, Talvinder S Sihra2, Jose Maria Delgado-Garcia1, and Antonio Rodriguez-Moreno1*

1 Department of Physiology, Anatomy and Cellular Biology, University Pablo de Olavide, Seville, Spain
2 Department of Pharmacology, UCL, London, United Kingdom

* To whom correspondence should be addressed. E-mail: arodmor{at}upo.es.

The mechanisms involved in the inhibition of glutamate release mediated by the activation of presynaptic kainate receptors (KARs) at the hippocampal mossy fiber-CA3 synapse are not well understood. We have observed a long-lasting inhibition of CA3 evoked excitatory postsynaptic currents (eEPSCs) following a brief application of kainate (KA) at concentrations ranging from 0.3 to 10 µM. The inhibition outlasted the change in holding current due to the activation of ionotropic KARs in CA3 pyramidal cells, indicating that this action is not contingent upon the opening of the receptor channels. The inhibition of the eEPSCs by KA was prevented by G-protein and protein kinase A (PKA) inhibitors and was enhanced after stimulation of the adenylyl cyclase (AC) with forskolin. We conclude that KARs present at mossy fiber terminals mediate the inhibition of glutamate release through a metabotropic mechanism that involves the activation of an AC-second messenger cAMP-PKA signaling cascade.




This article has been cited by other articles:


Home page
 J. Physiol.Home page
J. Yang, S. E. L. Chamberlain, G. L. Woodhall, and R. S. G. Jones
Mobility of NMDA autoreceptors but not postsynaptic receptors at glutamate synapses in the rat entorhinal cortex
J. Physiol., October 15, 2008; 586(20): 4905 - 4924.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. PsychiatryHome page
S. Paddock, G. Laje, D. Charney, A. J. Rush, A. F. Wilson, A. J.M. Sorant, R. Lipsky, S. R. Wisniewski, H. Manji, and F. J. McMahon
Association of GRIK4 With Outcome of Antidepressant Treatment in the STAR*D Cohort
Am J Psychiatry, August 1, 2007; 164(8): 1181 - 1188.
[Abstract] [Full Text] [PDF]

Home page
 J. Physiol.Home page
G. Grabauskas, B. Lancaster, V. O'Connor, and H. V. Wheal
Protein kinase signalling requirements for metabotropic action of kainate receptors in rat CA1 pyramidal neurones
J. Physiol., March 1, 2007; 579(2): 363 - 373.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 2006 by the The American Physiological Society.