Abstract
Posttraumatic stress disorder (PTSD) is a devastating, prevalent psychological disorder characterized by excessive fear memory because of exposure to severe trauma. Stellate ganglion block (SGB) is traditionally used as a clinical treatment for pain but has been regarded as an innovative therapy for PTSD in recent reports. However, the mechanisms underlying the effect of SGB on PTSD remain unknown. Here, we established a fear conditioning model, which is considered a representative model of traumatic memory, and evaluated the effect of SGB on conditioned fear memory. We found that SGB reduced conditioned fear memory in mice in conjunction with the hypoactivity of locus coeruleus (LC) noradrenergic and basolateral amygdala (BLA) glutamatergic neurons. The norepinephrine concentration in the BLA decreased after SGB. Moreover, conditioned fear memory was re-enforced when the LC NE (LC(NE))-BLA pathway was activated in SGB mice. Our study findings indicated that the hypoactivity of the LC(NE)-BLA pathway was the potential mechanism underlying the effects of SGB, which diminished consolidation of fear memory to relieve PTSD symptoms.