“…Next, we found that the negative indirect effect of pain intensity on QoL was through depression. The imaging studies on human found that many brain areas involved in pain and depression were overlaped, such as primary and secondary somatosensory cortex, anterior cingular cortex, hippocumpus and so on (Doan, Manders, & Wang, ; Green et al, ; Ushinsky, Reinhardt, Simmons, & Strigo, ; Zeng et al, ). Animal studies, based on NeP induced depression model, revealed that some common neuroplasticity changes were shared between pain and depression in central nerve system and the underlying mechanism included monoamine neurotransmitters, inflammatory factors and glutamate and its receptors (Doan et al, ; Humo, Lu, & Yalcin, ; Sheng, Liu, Wang, Cui, & Zhang, ).…”