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J Neurophysiol (July 25, 2007). doi:10.1152/jn.00473.2007
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Submitted on April 26, 2007
Accepted on July 16, 2007

LTP in the Hippocampal CA1 Region Does Not Require Insertion and Activation of GluR2-Lacking AMPA Receptors

Erin E. Gray1, Ann E. Fink1, Joshua Sarinana2, Bryce Vissel3, and Thomas J O'Dell2*

1 Interdepartmental Ph.D. Program for Neuroscience, UCLA, Los Angeles, California, United States
2 Physiology, David Geffen School of Medicine at UCLA, Los Angeles, California, United States
3 Neuroscience Program, Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia

* To whom correspondence should be addressed. E-mail: todell{at}mednet.ucla.edu.

Activity-dependent insertion of AMPA-type glutamate receptors is thought to underlie long-term potentiation (LTP) at Schaffer collateral fiber synapses on pyramidal cells in the hippocampal CA1 region. Although it is widely accepted that the AMPA receptors at these synapses contain GluR2 subunits, recent findings suggest that LTP in hippocampal slices obtained from 2 to 3 week old rodents is dependent on the transient postsynaptic insertion and activation of Ca2+-permeable, GluR2-lacking AMPA receptors. Here we examined whether LTP in slices prepared from adult animals exhibits similar properties. In contrast to previously reported findings, pausing synaptic stimulation for as long as 30 minutes post-LTP induction had no effect on LTP maintenance in slices from 2-3 month old mice. LTP was also not disrupted by post-induction application of a selective blocker of GluR2-lacking AMPA receptors or the broad spectrum glutamate receptor antagonist kynurenate. Although these results suggest that the role of GluR2-lacking AMPA receptors in LTP might be regulated during post-natal development, LTP in slices obtained from 15 to 21 day old mice also did not require post-induction synaptic stimulation or activation of GluR2-lacking AMPA receptors. Thus, the insertion and activation of GluR2-lacking AMPA receptors do not appear to be fundamental processes involved in LTP at excitatory synapses in the hippocampal CA1 region.




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