Our body feels like it is ours. However, individuals with body integrity identity disorder (BIID) lack this feeling of ownership for distinct limbs and desire amputation of perfectly healthy body parts. This extremely rare condition provides us with an opportunity to study the neural basis underlying the feeling of limb ownership, since these individuals have a feeling of disownership for a limb in the absence of apparent brain damage. Here we directly compared brain activation between limbs that do and do not feel as part of the body using functional MRI during separate tactile stimulation and motor execution experiments. In comparison to matched controls, individuals with BIID showed heightened responsivity of a large somatosensory network including the parietal cortex and right insula during tactile stimulation, regardless of whether the stimulated leg felt owned or alienated. Importantly, activity in the ventral premotor cortex depended on the feeling of ownership and was reduced during stimulation of the alienated compared to the owned leg. In contrast, no significant differences between groups were observed during the performance of motor actions. These results suggest that altered somatosensory processing in the premotor cortex is associated with the feeling of disownership in BIID, which may be related to altered integration of somatosensory and proprioceptive information.

The dentate gyrus (DG) is crucial for behaviorally discriminating similar spatial memories, predicting that DG place cells change ("remap") their relative spatial tuning ("place fields") for memory discrimination. This prediction was never tested, although DG place cells remap across similar environments without memory tasks. We confirm this prior finding but find that DG place fields do not remap across spatial tasks that require DG-dependent memory discrimination. Instead of remapping, place-discriminating discharge is observed transiently among DG place cells, particularly when memory discrimination is most necessary. The DG network may signal memory discrimination by expressing distinctive sub-second network patterns of co-firing at memory discrimination sites. This involves increased coupling of discharge from place cells and interneurons, as was observed during successful, but not failed, behavioral expression of memory discrimination. Instead of remapping, these findings indicate that memory discrimination is signaled by sub-second patterns of correlated discharge within the dentate network.