2-Heptanone increases the firing rate of the basal amygdala: role of anterior olfactory epithelial organs.

Wistar rats subjected to physical stress release a urine alarm pheromone (2-heptanone) that produces signs of anxiety and despair in receptor rats not subjected to physical stress. However, unknown are the effects of 2-heptanone on the firing rate of the basal amygdala, a structure that participates in the expression of fear, and the participation of anterior olfactory epithelial organs, namely the septal organ and vomeronasal organ (SO-VNO). We explored the effects of 2-heptanone applied near the nostrils on single-unit extracellular recordings from the basal amygdala in a sham-operated group and rats that underwent removal of the SO-VNO. The firing rate of basal amygdala neurons in the SO-VNO removal group was significantly higher than in the sham-operated group. In both groups, recordings were classified according to the responses to 2-heptanone (i.e., increased firing rate, decreased firing rate, and no response). SO-VNO removal was associated with an increased firing rate in the three types of neurons. A similar number of neurons increased their firing rate during and after 2-heptanone stimulation in both groups, but such an increase in firing rate was longer in the group of rats subjected to SO-VNO removal. The results indicate that the SO-VNO is not essential for the effect of 2-heptanone on the firing rate of basal amygdala neurons. SO-VNO ablation did not block but rather accentuated the response of amygdala neurons to 2-heptanone.