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The Journal of Neuroscience, April 29, 2009, 29(17):5587-5596; doi:10.1523/JNEUROSCI.5314-08.2009

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Cellular/Molecular
Activity Pattern-Dependent Long-Term Potentiation in Neocortex and Hippocampus of GluA1 (GluR-A) Subunit-Deficient Mice

Marco C. Frey,¹ Rolf Sprengel,² and Thomas Nevian^1,3

¹Department of Cell Physiology and ²Department of Molecular Neurobiology, Max Planck Institute for Medical Research, D-69120 Heidelberg, Germany, and ³Department of Physiology, University of Berne, CH-3012 Bern, Switzerland

Correspondence should be addressed to Thomas Nevian, Department of Physiology, University of Berne, Bühlplatz 5, CH-3012 Bern, Switzerland. Email: nevian{at}pyl.unibe.ch

The AMPA receptor subunit GluA1 (GluR-A) has been implicated to be critically involved in the expression of long-term potentiation (LTP) and memory formation. Mice lacking this subunit possess a profound spatial working memory deficit. We investigated the influence of the GluA1 subunit on the expression of LTP in pyramidal neurons of the hippocampus CA1 region and somatosensory cortex layer 2/3 for different cellular LTP protocols in adult mice. We found that the GluA1 subunit was not required for LTP in cortical pyramidal neurons. In contrast, GluA1-dependent LTP expression in CA1 pyramidal neurons was differentially dependent on the LTP induction parameters. Depolarization pairing was exclusively, theta-burst pairing was partially, and spike-timing-dependent plasticity (STDP) was independent of the GluA1 subunit. Spike-timing-dependent LTP required postsynaptic membrane fusion in CA1 pyramidal neurons. We conclude that during LTP induction at the hippocampal CA3-to-CA1 synapse the recruitment of the GluA1 subunit is controlled by particular electrical activity patterns that might reflect specific behavioral states. Furthermore, other LTP expression mechanisms exist that do not require the presence of GluA1. The previously reported spatial working memory deficits in GluA1-lacking mice (Gria1^–/– mice) together with these results suggest that STDP might be a likely basis for the formation of spatial reference memory whereas it is not required for the rapid formation of spatial working memory where a fast but transient increase of synaptic efficacy might be needed.

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Received Nov. 5, 2008; revised March 11, 2009; accepted March 31, 2009.

Correspondence should be addressed to Thomas Nevian, Department of Physiology, University of Berne, Bühlplatz 5, CH-3012 Bern, Switzerland. Email: nevian{at}pyl.unibe.ch

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