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First published online on October 10, 2003.
 Copyright © 2003 by The Physiological Society
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jphysiol.2003.053637v1
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Rolf Sprengel
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Received August 19, 2003
Revised September 4, 2003
Accepted after revision October 8, 2003

A juvenile form of postsynaptic hippocampal LTP in mice deficient for the AMPA receptor subunit GluR-A

Vidar Jensen1, Katherina M.M. Kaiser2, Thilo Borchardt3, Giselind Adelmann4, Andrei Rozov5, Nail Burnashev6, Christian Brix7, Michael Frotscher7, Per Andersen8, Øivind Hvalby1, Bert Sakmann9, Peter H Seeburg3, and Rolf Sprengel3*

1 Department of Physiology, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway
2 Department of Cell Physiology, Max-Planck-Institute for Medical Research, Heidelberg, Germany
3 Department of Molecular Neurobioly, Max-Planck-Institute for Medical Research, Heidelberg, Germany
4 Institute of Anatomy, University of Freiburg
5 Clinical Neurobiology, University of Heidelberg, INF 264, D-69120 Heidelberg, Germany
6 Department of Neurophysiology, Faculty of Biology, Vrije University, 1081 HV Amsterdam, Netherlands
7 Institute of Anatomy, University of Freiburg, Albertstrasse 17, D-79104-Freiburg, Germany
8 Department of Physiology, Institute of Basic Medical Sciences, University of Oslo, Norway
9 Department of Cell Physiology, Max-Planck-Institute for Medical Research, Heidelberg, Germany,

* To whom correspondence should be addressed. E-mail: sprengel{at}mpimf-heidelberg.mpg.de.

In adult mice, long-term potentiation (LTP) of synaptic transmission at CA3-to-CA1 synapses induced by tetanic stimulation requires L-a-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors containing GluR-A subunits. Here, we report a GluR-A independent form of LTP, which is comparable in size to LTP in wild-type mice at postnatal day 14 (P14) but diminishes between P14 and P42 in brain slices of GluR-A deficient mice. The GluR-A independent LTP is sensitive to D-AP5, but lacks short-term potentiation (STP) and can also be observed in the pairing induction protocol. As judged by unaltered paired-pulse facilitation, this LTP form is postsynaptically expressed despite depleted extrasynaptic AMPA receptor pools with reduced levels of GluR-B immunoreactivity, which accumulates in somata and synapses of CA1 pyramidal neurons in GluR-A deficient mice. Our results show that in the developing hippocampus synaptic plasticity can be expressed by AMPA receptors lacking the GluR-A subunit.


Key words: AMPA receptor • LTP • Memory






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