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Publication : Transgenic mice lacking NMDAR-dependent LTD exhibit deficits in behavioral flexibility.

First Author  Nicholls RE Year  2008
Journal  Neuron Volume  58
Issue  1 Pages  104-17
PubMed ID  18400167 Mgi Jnum  J:135145
Mgi Id  MGI:3790528 Doi  10.1016/j.neuron.2008.01.039
Citation  Nicholls RE, et al. (2008) Transgenic mice lacking NMDAR-dependent LTD exhibit deficits in behavioral flexibility. Neuron 58(1):104-17
abstractText  While most studies have focused on the role of long-term potentiation in behavior, far less is known about the role of long-term depression (LTD). To examine the potential involvement of LTD in learning and memory, we generated transgenic mice that express a fragment of the SV40 small t antigen known to inhibit protein phosphatase 2A (PP2A). Small t antigen expression blocked both stimulus-induced and chemically induced NMDAR-dependent LTD at Schaffer collateral synapses but did not affect potentiation, depotentiation, or mGluR-dependent LTD. This physiological phenotype was associated with deficits in behavioral flexibility in both the Morris water maze and a delayed nonmatch to place T-maze task, suggesting that NMDAR-dependent LTD is required for behavioral flexibility and may act by weakening previously encoded memory traces when new information is learned.
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