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First published online on July 23, 2003.
 Copyright © 2003 by The Physiological Society
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Received April 21, 2003
Revised June 2, 2003
Accepted after revision July 23, 2003

Impaired regulation of synaptic strength in hippocampal neurons from GluR1-deficient mice

Bertalan K Andrįsfalvy1*, Mark A Smith1, Thilo Borchardt2, Rolf Sprengel2, and Jeffrey C Magee1

1 LSU Health Science Center
2 Max-Planck Institute for Medical Research

* To whom correspondence should be addressed. E-mail: bandra{at}lsuhsc.edu.

Neurons of the central nervous system (CNS) exhibit a variety of forms of synaptic plas-ticity; including associative long-term potentiation and depression (LTP/D), homeostatic activity-dependent scaling and distance-dependent scaling. A regulation of synaptic neurotransmitter receptors is currently thought to be a common mechanism among many of these forms of plasticity. In fact, glutamate receptor 1 (GluR1 or GluRA) subunit containing L-a-amino-3-hydroxy-5- methylisoxazle-4-propionate (AMPA) receptors have been shown to be required for several forms of hippocampal LTP and a particular hippocampal-dependent learning task. Because of this importance in associative plasticity, we sought to examine the role of these receptors in other forms of synaptic plasticity in the hippocampus. To do so, we recorded from the apical dendrites of hippocampal CA1 pyramidal neurons in mice lacking the GluR1 subunit (GluR1 -/-). Here we report data from outside-out patches that indicate GluR-1 containing receptors are essential to the extra-synaptic population of AMPA receptors, as this pool was nearly empty in the GluR1 -/- mice. Additionally, these receptors appear to be a significant component of the synaptic glutamate receptor pool as well because the amplitude of spontaneous synaptic currents recorded at the site of input and synaptic AMPA receptor currents evoked by focal glutamate un-caging were both substantially reduced in these mice. Interestingly, the impact on synaptic weight was greatest at distant synapses such that the normal distance-dependent synaptic scaling used by these cells to counter dendritic attenuation was lacking in GluR1 -/- mice. Together the data suggest that the highly regulated movement of GluR1 containing AMPA receptors between extra-synaptic and synaptic receptor pools is critically involved in establishing two functionally diverse forms of synaptic plasticity; LTP and distance-dependent scaling.


Key words: AMPA receptor • Dendrite • Plasticity




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