Vasopressin decreases excitability in rat lateral amygdala neurons through inhibition of hyperpolarization-activated cationic current.

The amygdala is a critical part of the limbic system with important roles in social behavior. Abnormal activity in the lateral amygdala nucleus (LA) has been implicated in several disorders, including autism spectrum disorder (ASD) in which abnormal social functioning is a primary symptom. The peptide hormones arginine-vasopressin (AVP) and oxytocin (OT) are strongly implicated in social behavior, and may also be involved in the pathophysiology of ASD. Here, we show that AVP causes an increase in excitability, through eliciting a decrease in action potential accommodation and hyperpolarization-activated current (Ih) amplitude in LA pyramidal cells. OT exerts complementary effects, causing an increase in action potential accommodation and Ih amplitude, resulting in decreased excitability. These results suggest AVP and OT may modulate social behavior by controlling excitability in the amygdala.