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Obsessive-compulsive disorder (OCD) affects ∼1 to 3% of the world’s population. However, the neural mechanisms underlying the excessive checking symptoms in OCD are not fully understood. Using viral neuronal tracing in mice, we found that glutamatergic neurons from the basolateral amygdala (BLAGlu) project onto both medial prefrontal cortex glutamate (mPFCGlu) and GABA (mPFCGABA) neurons that locally innervate mPFCGlu neurons. Next, we developed an OCD checking mouse model with quinpirole-induced repetitive checking behaviors. This model demonstrated decreased glutamatergic mPFC microcircuit activity regulated by enhanced BLAGlu inputs. Optical or chemogenetic manipulations of this maladaptive circuitry restored the behavioral response. These findings were verified in a mouse functional magnetic resonance imaging (fMRI) study, in which the BLA–mPFC functional connectivity was increased in OCD mice. Together, these findings define a unique BLAGlu→mPFCGABA→Glu circuit that controls the checking symptoms of OCD.

Fig. 1 BLAGlu neurons preferentially synapse on mPFCGABA.

The pathophysiology underlying obsessive-compulsive disorder (OCD) remains unclear, leading to major challenges in the treatment of OCD patients. Using viral neuronal tracing in mice, the authors define a critical BLA^Glu→mPFC^GABA→Glu circuit through which compulsive checking behavior is generated. A mechanistic functional understating of this circuit will provide insight into the possible mechanisms underlying human OCD checking symptoms.
 
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