Exposure to an Alarm Pheromone Combined with Footshock Stress Enhances Responsivity of the Medial Amygdala-Hippocampus Circuit

Abstract

Alarm substances are released under stressful situations and may constitute signals that prevent other members of the group from encountering dangerous situations by producing fear. 2-Heptanone is an alarm pheromone that increases the neuronal firing rate in temporal lobe structures that are related to fear in the rat, such as the basal amygdala. A single stress session of unavoidable electric footshock or 2-heptanone sniffing increases the responsivity of the medial amygdala-hippocampus circuit, but unknown is the timing of action of simultaneous exposure to both stressors on the firing rate and responsivity of CA1-CA3 neurons identified by their connections with the medial amygdala nucleus. Twenty-four or 48 h after a single stress session, we obtained single-unit extracellular recordings. The firing rate was higher in the 48 h group. The peristimulus histogram showed an increase in the responsivity of amygdala-hippocampus neurons, which was more pronounced 48 h after a single stress session. The present results suggest an increase in the sensitivity of this circuit after a single stress session, seemingly representing a first step in the formation of emotional memories related to a conditioned response to fear.