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Olfactory dysfunction has become a predictor of impaired social behaviors and associated neuropsychiatric conditions, though the mechanisms behind this are not well understood. In this context, we have been using the social isolation model in mice to investigate how sociability may influence olfaction. In this talk, I’ll show data using male CD-1 (ICR) mice that were kept in groups (GH) or individually (SI) in their home cages for 7 days. Olfaction was examined on two levels. First, we performed whole-cell patch-clamp recordings in the mitral cell layer (MCL) of the olfactory bulb (OB), which contains the primary output neurons that convey processed odor information to higher-order brain regions. To distinguish mitral (MC) from deep tufted (TC) cells, we applied a method based on membrane resistance. Afterward, we compared the passive and active properties of both cell populations between SI and GH animals. SI decreased the rheobase of MC but increased that of TC, indicating a cell-type-specific effect rather than a globally excitatory or inhibitory effect. The olfaction was also estimated at the behavioral level. SI mice had altered the spatial localization and novelty detection of social odors. Furthermore, we chose two paradigms that rely on olfaction to produce long-term memories: social discrimination and olfactory fear conditioning. Mice that underwent SI could not distinguish familiar from novel conspecifics and showed reduced freezing in response to an odor previously paired with a footshock, indicating an olfactory memory deficit. Our data suggest that briefly abolishing social interactions can reorganize the excitability of output neurons in the OB, probably reshaping the flow of odor information. The observation that SI also alters olfactory function at the behavioral level encourages future studies to explore whether excitability in the OB is linked to olfactory deficits under social isolation.
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