Stress-induced dorsal raphe serotonin activation immediately after maternal separation stress in mice

Early-life stress produces cognitive and emotional symptoms contributing to the etiology of psychiatric disorders, like anxiety and depression. In rodents, many of these symptoms are replicated in a model of early-life stress when pups are subjected to a repeated maternal separation protocol [3hs/day from postnatal day (p) 2 to 14]. Maladaptive changes in this model impact brain circuit development and maturation. While it is thought that serotonin could play a role in this mechanism, very little is known about its potential role. We investigate in this model, if early-life stress through serotonin can modify the capacity of serotoninergic neurons to respond to a mild stress immediately after the end of stress exposure (at p15). To this purpose, we exposed C57BL/6 mice to maternal separation while administering a specific inhibitor of the serotonin synthesis enzyme, Tryptophan hydroxylase, or saline, during the postnatal critical period (p2-14). On the next day, after treatment cessation (p15), mice were subjected to the forced swim test to study dorsal raphe serotonin neuron activation using cFos immunofluorescence and confocal microscopy. Our preliminary results suggest that serotonin could have a crucial role in mediating the effects of early-life stress on the raphe network engaged in stress-coping behavioral strategies.