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Brain serotonin (5-HT) system dysfunction is implicated in depressive disorders and acute depletion of 5-HT precursor tryptophan has frequently been used to model the influence of 5-HT deficiency on emotion regulation. Tamoxifen (TAM)-induced Cre/loxP-mediated inactivation of the tryptophan hydroxylase-2 gene ( Tph2 ) was used to investigate the effects of provoked 5-HT deficiency in adult mice ( Tph2  icKO) previously subjected to maternal separation (MS). The efficiency of Tph2 inactivation was validated by immunohistochemistry and HPLC. The impact of  Tph2  icKO in interaction with MS stress ( Tph2  icKO × MS) on physiological parameters, emotional behavior and expression of 5-HT system-related marker genes were assessed.  Tph2  icKO mice displayed a significant reduction in 5-HT immunoreactive cells and 5-HT concentrations in the rostral raphe region within four weeks following TAM treatment.  Tph2  icKO and MS differentially affected food and water intake, locomotor activity as well as panic-like escape behavior.  Tph2  icKO prevented the adverse effects of MS stress and altered the expression of the genes previously linked to stress and emotionality. In conclusion, an experimental model was established to study the behavioral and neurobiological consequences of 5-HT deficiency in adulthood in interaction with early-life adversity potentially affecting brain development and the pathogenesis of depressive disorders.

Serotonin deficiency induced after brain maturation rescues consequences of early life adversity