A) We suggest that acute anxiogenic stimuli activate neurons in the anterolateral BNST, thereby increasing levels of CRF within the caudal DRN. The release of CRF within the caudal DRN excites a subpopulation of 5-HT neurons projecting to the BNST, and in turn increases levels of 5-HT within the BNST. 5-HT release in the BNST preferentially acts on 5-HT1A receptors to reduce BNST activity. B) In a state of pathological anxiety, we suggest that exposure to stress may downregulate 5-HT1A receptor function and/or upregulate 5-HT2A, 5-HT2C, and/or 5-HT7 function, thereby shifting the balance of these receptors towards excitation. Hence, the normal negative-feedback role of BNST 5-HT release is compromised, increasing anxiety.