Anterior olfactory organ removal produces anxiety-like behavior and increases spontaneous neuronal firing rate in basal amygdala

• Septal–vomeronasal organs (SO–VNO) lesion produces neuronal devastation in AOB.
• An enhanced neuronal firing rate in the basal amygdala follows SO–VNO lesion.
• SO–VNO lesion increases anxiety-like behavior in the elevated plus maze.
• SO–VNO lesion increases self-directed behaviors in the social interaction test.
• Anterior epithelial olfactory structures participate in the modulation of anxiety.

Some chemical cues may produce signs of anxiety and fear mediated by amygdala nuclei, but unknown is the role of two anterior olfactory epithelial organs, the septal and vomeronasal organs (SO–VNOs). The effects of SO–VNO removal were explored in different groups of Wistar rats using two complementary approaches: (i) the assessment of neuronal firing rate in basal and medial amygdala nuclei and (ii) behavioral testing. Fourteen days after SO–VNO removal, spontaneous activity in basal and medial amygdala nuclei in one group was determined using single-unit extracellular recordings. A separate group of rats was tested in the elevated plus maze, social interaction test, and open field test. Compared with sham-operated and intact control rats, SO–VNO removal produced a higher neuronal firing rate in the basal amygdala but not medial amygdala. In the behavioral tests, SO–VNO removal increased signs of anxiety in the elevated plus maze, did not alter locomotion, and increased self-directed behavior, reflecting anxiety-like behavior. Histological analysis showed neuronal destruction in the accessory olfactory bulb but not anterior olfactory nucleus in the SO–VNO group. The present results suggest the participation of SO–VNO/accessory olfactory bulb/basal amygdala relationships in the regulation of anxiety through a process of disinhibition.