Abstract

The NMDA receptor plays a key role in synaptic plasticity and its disruption leads to impaired spatial representation in the CA1 area of the hippocampus, with place cells exhibiting larger place fields (McHugh et al., 1996). Place fields are defined by the spatial and nonspatial inputs of a given place and context, by intrinsic network processes, such as phase precession, but also by the matching of these inputs to a pre-existing spatial representation. Larger place fields may be a consequence of spatially widened firing upon a single crossing of a place field, or of increased variability in place field positions across traversals. We addressed this question by monitoring CA1 place cell activity, with tetrodes, in control and KO mice lacking the NMDA receptor in this region. In individual crossings of the field, we found no difference between genotypes in place field size; the larger, overall place field size turns out to be a consequence of jitter across trials. We suggest that this jitter reflects a deficit in the matching of current spatial inputs to the stored spatial representation of the track. This is supported by the finding that deficits in place field size and spatial information are rescued by extensive exposure of the mouse to the track, which may echo an increased influence of memory retrieval processes in CA3 on firing in CA1.