Figure 1. An interpeduncular nucleus (IPN) microcircuit is regulated by dopamine to drive anxiety-like behavior.

DeGroot et al. (2020) present an elegant set of studies showing that increasing dopamine in the IPN regulates microcircuit activity to drive the expression of anxiety-like behavior. (A) Optically activating ventral tegmental area (VTA) processes in the IPN increased anxiety-like behavior in rodents. Inhibition of these processes had an anxiolytic effect (not shown). (B) Proposed circuit mechanism of dopaminergic regulation of the IPN. Dopamine released in the caudal IPN (cIPN) activates D1 receptors on GABAergic neurons (Type C neurons) that project to the ventral (vIPN) to regulate presynaptic release probability of excitatory inputs. Depending on the input this either increases (left) or decreases (right) release probability to increase (Type A neurons) or decrease (Type B neurons) cellular activity in two morphologically distinct cellular populations downstream. The authors suggest that this occurs through a monosynaptic mechanism where GABA_B receptors on Type A inputs enhance glutamate release probability – an effect that has been observed in other circuits (7) -, while GABA receptors on Type B inputs reduce release probability. Created with BioRender.com