Abstract
Early life adversity (ELA) significantly increases the later risk for depression. In humans, depression has been associated with disturbances in the hedonic perception of odorants. As olfaction serves a primary role in social interactions, food intake, and daily pleasures, altered olfactory perception and hedonic processing of chemosensory cues may provide insights into basic neurobiological disturbance in ELA-associated pathology as well as identify key pathways that can impact on quality of life, contributing to the development and severity of depressive pathology. Here, we used the limited bedding and nesting protocol in mice to model ELA in the form of fragmented maternal care. The aim of this study was to determine whether ELA altered the hedonic processing of odorants, and to identify neural substrates underlying those effects. We found that ELA led to a specific reduction in the investigation of pleasant odorants. Using cellular imaging and fine structural analysis of neurons, we found altered morphology of the neurons responding specifically to pleasant odorants in the olfactory bulb, and an altered activity in the olfactory tubercle and ventral tegmental area, key structures implicated in the hedonic coding of odorants. These results highlight potential impacts of ELA on network development and response to exogenous signals, diminishing interest in hedonically pleasant odorants. The current results point to ELA altering the neural substrates implicated in basic olfactory sensory function and reward, with implications for understanding broader risk for anhedonia and symptom severity in individuals at risk for depression associated with prior history of ELA.