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Neural Plasticity
Volume 2008 (2008), Article ID 840374, 9 pages
Research Article

Postsynaptic Signals Mediating Induction of Long-Term Synaptic Depression in the Entorhinal Cortex

1Center for Studies in Behavioral Neurobiology, Department of Psychology, Concordia University, Montréal, QC, Canada H4B 1R6
2Departments of Neuroscience and Psychology and the Institute of Human Genetics, University of Minnesota, Minneapolis, MN 55455, USA

Received 17 December 2007; Accepted 24 April 2008

Academic Editor: Roland S. G. Jones

Copyright © 2008 Saïd Kourrich et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The entorhinal cortex receives a large projection from the piriform cortex, and synaptic plasticity in this pathway may affect olfactory processing. In vitro whole cell recordings have been used here to investigate postsynaptic signalling mechanisms that mediate the induction of long-term synaptic depression (LTD) in layer II entorhinal cortex cells. To induce LTD, pairs of pulses, using a 30-millisecond interval, were delivered at 1 Hz for 15 minutes. Induction of LTD was blocked by the NMDA receptor antagonist APV and by the calcium chelator BAPTA, consistent with a requirement for calcium influx via NMDA receptors. Induction of LTD was blocked when the FK506 was included in the intracellular solution to block the phosphatase calcineurin. Okadaic acid, which blocks activation of protein phosphatases 1 and 2a, also prevented LTD. Activation of protein phosphatases following calcium influx therefore contributes to induction of LTD in layer II of the entorhinal cortex.