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J Physiol Volume 584, Number 3, 885-894, November 1, 2007 DOI: 10.1113/jphysiol.2007.137380
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NEUROSCIENCE

NMDA receptor-dependent long-term potentiation in mouse hippocampal interneurons shows a unique dependence on Ca2+/calmodulin-dependent kinases

 Karri Lamsa1, Elaine E. Irvine2, K. Peter Giese2 and Dimitri M. Kullmann1

1 Institute of Neurology
2 Wolfson Institute for Biomedical Research, University College London

Long-term potentiation (LTP) of excitatory synaptic transmission plays a major role in memory encoding in the cerebral cortex. It can be elicited at many synapses on principal cells, where it depends on Ca2+ influx through postsynaptic N-methyl-D-aspartic acid (NMDA) receptors. Ca2+ influx triggers phosphorylation of several kinases, in particular Ca2+/calmodulin-dependent kinase type II (CaMKII). Auto-phosphorylation of CaMKII is a key step in the LTP induction cascade, as revealed by the absence of LTP in hippocampal pyramidal neurons of {alpha}CaMKII T286A-mutant mice, where auto-phosphorylation of the {alpha} isoform at residue T286 is prevented. A subset of hippocampal interneurons mediating feed-forward inhibition also exhibit NMDA receptor-dependent LTP, which shows all the cardinal features of Hebbian LTP in pyramidal neurons. This is unexpected, because {alpha}CaMKII has not been detected in interneurons. Here we show that pathway-specific NMDA receptor-dependent LTP is intact in hippocampal inhibitory interneurons of {alpha}CaMKII T286A-mutant mice, although in pyramidal cells it is blocked. However, LTP in interneurons is blocked by broad-spectrum pharmacological inhibition of Ca2+/calmodulin-dependent kinases. The results suggest that non-{alpha} Ca2+/calmodulin-dependent kinases substitute for the {alpha} isoform in NMDA receptor-dependent LTP in interneurons.

(Received 25 May 2007; accepted after revision 3 September 2007; first published online 20 September 2007)
Corresponding author D. M. Kullmann: Institute of Neurology, University College London, Queen Square, London, WC1N 3BG, UK. Email: d.kullmann{at}ion.ucl.ac.uk

This paper has online supplemental material.






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