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J. Biol. Chem., Vol. 282, Issue 25, 18100-18107, June 22, 2007

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Learning-induced Glutamate Receptor Phosphorylation Resembles That Induced by Long Term Potentiation^*

From the Departments of Neurology and Psychiatry, The University of Texas Southwestern Medical Center, Dallas, Texas 75390-8813

Long term potentiation and long term depression of synaptic responses in the hippocampus are thought to be critical for certain forms of learning and memory, although until recently it has been difficult to demonstrate that long term potentiation or long term depression occurs during hippocampus-dependent learning. Induction of long term potentiation or long term depression in hippocampal slices in vitro modulates phosphorylation of the -amino-3-hydrozy-5-methylisoxazole-4-propionic acid subtype of glutamate receptor subunit GluR1 at distinct phosphorylation sites. In long term potentiation, GluR1 phosphorylation is increased at the Ca²⁺/calmodulin-dependent protein kinase and protein kinase C site serine 831, whereas in long term depression, phosphorylation of the protein kinase A site serine 845 is decreased. Indeed, phosphorylation of one or both of these sites is required for long term synaptic plasticity and for certain forms of learning and memory. Here we demonstrate that training in a hippocampus-dependent learning task, contextual fear conditioning is associated with increased phosphorylation of GluR1 at serine 831 in the hippocampal formation. This increased phosphorylation is specific to learning, has a similar time course to that in long term potentiation, and like memory and long term potentiation, is dependent on N-methyl-D-aspartate receptor activation during training. Furthermore, the learning-induced increase in serine 831 phosphorylation is present at synapses and is in heteromeric complexes with the glutamate receptor subunit GluR2. These data indicate that a biochemical correlate of long term potentiation occurs at synapses in receptor complexes in a final, downstream, postsynaptic effector of long term potentiation during learning in vivo, further strengthening the link between long term potentiation and memory.

Received for publication, April 5, 2007 , and in revised form, April 30, 2007.

^* This work was supported by National Institutes of Health Grant MH65975 and by National Alliance for Research on Schizophrenia and Depression Young Investigator Award 2003 Leiber Investigator (to C. M. P.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement"in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed: Dept. of Neurology, UT Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-8813. Tel.: 214-645-6251; Fax: 214-645-6240; E-Mail: craig.powell{at}utsouthwestern.edu.

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