Data from mice that only underwent SDT are shown as gray lines and blank circles, while data from mice that also underwent electrophysiological recordings from vCA1 are shown as black lines and filled circles. Comparison of duration spent in the social zone ( c) and the discrimination score ( d). Note that the map for Trial 2 is rotated and superposed onto that of Trial 1. b Heat map of occupancy time during Trial 1 and Trial 2 from a representative session. Dotted lines in the arena indicate the borders of social zones. After 2 h of familiarization between a subject mouse (S) and a stimulator mouse-A in a home cage, the subject mouse was allowed to explore a social arena where the familiar mouse-A and a novel mouse-B were placed. These results suggest that SPW-R-mediated sequential reactivation of neuronal ensembles is a canonical mechanism for coordinating hippocampus-dependent social memories and its disruption underlie the pathophysiology of social memory defects associated with ASD.Ī Schematic of the behavioral paradigm. In ASD model Shank3 knockout mice, the proportion of social memory neurons was reduced, and neuronal ensemble spike sequences during SPW-Rs were disrupted, which correlated with impaired discriminatory social behavior. Spike sequences of these social replays reflected the temporal orders of neuronal activities within theta cycles during social experiences. Here we show that vCA1 social memory neurons, characterized by enhanced activity in response to memorized individuals, were preferentially reactivated during sharp-wave ripples (SPW-Rs). Although hippocampal ventral CA1 (vCA1) neurons are known to store social memories, how their activities are coordinated remains unclear. The ability to remember conspecifics is critical for adaptive cognitive functioning and social communication, and impairments of this ability are hallmarks of autism spectrum disorders (ASDs).
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