There is evidence for stressor- and brain region-specific selectivity in serotonergic transmission responses to aversive stimuli. The aim of the present review is to provide an overview of the effects of different acute and repeated/chronic stressors on serotonin (5-HT) release and reuptake, extracellular 5-HT levels, and 5-HT pre- and postsynaptic receptors in areas tightly linked to the control of fear and anxiety, namely the dorsal and median raphe nuclei, the frontal cortex, the amygdala and the hippocampus. In addition, our knowledge of the impacts of corticoids on serotonergic systems in these brain areas is also briefly provided to examine whether the hypothalamo-pituitary-adrenal axis may play a role in stress-induced alterations in 5-HT neurotransmission. Taken together, the data presented reinforce the hypothesis that stress affects such a transmission, partly through the actions of corticoids. However, we are still left with unanswered, albeit crucial questions. First, the question of the specificity of the serotonergic responses to stress, with regard to the site of action and the nature of the stressor still remains open due to the heterogeneity of the results obtained so far. This could indicate that environmental factors, other than the stressor itself, may have enduring consequences on 5-HT sensitivity to stress. Second, the question regarding the role of stress-elicited changes in 5-HT transmission within coping processes finds in most cases no clearcut answer. In keeping with human symptomatology, the need to consider the environment (including the early one) and the genetic status when assessing the effects of stress on 5-HT neurotransmission is underlined. Such a consideration could help to answer the questions raised.