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SYMPOSIUM REPORT |
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
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