Down Syndrome (DS) in humans is caused by trisomy of chromosome 21 and is marked by prominent difficulties in learning and memory. Decades of research have demonstrated that the hippocampus is a key structure in learning and memory, and recent work with mouse models of DS has suggested differences in hippocampal activity that may be the substrate of these differences. One of the primary functional differences in DS is thought to be an excess of GABAergic innervation from Medial Septum (MS) to the hippocampus. In these experiments, we probe in detail the activity of region CA1 of the hippocampus using in vivo electrophysiology in male Ts65Dn mice, in comparison to their male non-trisomic 2N littermates. We find the spatial properties of place cells in CA1 are normal in Ts65Dn animals. However we find that the phasic relationship of both CA1 place cells and gamma rhythms to theta rhythm in the hippocampus are profoundly altered in these mice. Since the phasic organisation of place cell activity and gamma osc...