J Physiol Society Membership
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Physiol Volume 586, Number 6, 1481-1486, March 15, 2008 DOI: 10.1113/jphysiol.2007.148064
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
586/6/1481    most recent
jphysiol.2007.148064v1
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 Kullmann, D. M.
Right arrow Articles by Lamsa, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kullmann, D. M.
Right arrow Articles by Lamsa, K.
Related Collections
Right arrow Review articles
Right arrow Neuroscience

SYMPOSIUM REPORT

Roles of distinct glutamate receptors in induction of anti-Hebbian long-term potentiation

Dimitri M. Kullmann1 and Karri Lamsa2

1 UCL Institute of Neurology, University College London, Queen Square, London WC1N 3BG, UK
2 Department of Pharmacology, Oxford University, Mansfield Road, Oxford OX1 3QT, UK

Many glutamatergic synapses on interneurons involved in feedback inhibition in the CA1 region of the hippocampus exhibit an unusual form of long-term potentiation (LTP) that is induced only if presynaptic glutamate release occurs when the postsynaptic membrane potential is relatively hyperpolarized. We have named this phenomenon ‘anti-Hebbian’ LTP because it is prevented by postsynaptic depolarization during afferent activity, and hence its induction requirements are opposite to those of Hebbian NMDA receptor-dependent LTP. This symposium report addresses the roles of distinct glutamate receptors in the induction of anti-Hebbian LTP. Inwardly rectifying Ca2+-permeable AMPA receptors mediate fast glutamatergic signalling at synapses that exhibit this form of LTP, and they are highly likely to mediate the instructive signal that triggers the cascade leading to synapse strengthening. NMDA receptors, on the other hand, play no role, nor do they contribute substantially to synaptic transmission at synapses that exhibit anti-Hebbian LTP. Both kainate and group I metabotropic glutamate receptors are abundant in at least some interneurons in the feedback inhibitory circuit. Delineating the roles of kainate receptors has been hampered by sub-optimal pharmacological tools. As for group I metabotropic glutamate receptors, their role in anti-Hebbian LTP is permissive at the very least in some interneuron types, although an instructive role has been suggested in other forms of activity-dependent plasticity.

(Received 9 November 2007; accepted after revision 28 December 2007; first published online 10 January 2008)
Corresponding author D. M. Kullmann: UCL Institute of Neurology, University College London, Queen Square, London WC1N 3BG, UK. Email: d.kullmann{at}ion.ucl.ac.uk


This report was presented at The Journal of Physiology Symposium on Synaptic Plasticity, San Diego, CA, USA, 2 November 2007. It was commissioned by the Editorial Board and reflects the views of the author.




This article has been cited by other articles:


Home page
J. Physiol.Home page
C. J. McBain
New directions in synaptic and network plasticity - a move away from NMDA receptor mediated plasticity
J. Physiol., March 15, 2008; 586(6): 1473 - 1474.
[Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2008 The Physiological Society.