The anterior cingulate cortex contributes to the analgesic rather than the anxiolytic effects of duloxetine in chronic pain-induced anxiety.

Mood disorders, such as anxiety and depression, are commonly found in people suffering from chronic pain. Serotonin-norepinephrine reuptake inhibitors (SNRIs) are potential in alleviating chronic pain and are the first-line option for anxiety disorder. The anterior cingulate cortex (ACC) plays a vital role in chronic pain-induced anxiety, but its role in the therapeutic effects of SNRIs remains largely unclear.

Fluoxetine reverses hyperactivity of anterior cingulate cortex and attenuates chronic stress-induced hyperalgesia.

Somatic symptom disorder (SSD), which occurs in about 5-7 percent of the adult population, involves heightened physical and emotional sensitivity to pain. However, its neural mechanism remains elusive and thus hinders effective clinical intervention. In this study, we employed chronic restraint stress (CRS)-induced hyperalgesia as a mouse model to investigate the neural mechanism underlying SSD and its pharmacological treatment.