4. Discussion
The current study aimed to determine the underlying physiological processes and cognitive mechanisms of stress-related impairment of creativity from a neuroendocrine perspective. We explored the effects of HPA axis and SAM axis activation on creativity under stress through an experimental study using reliable biomarkers. Importantly, the mediating role of cognitive flexibility in the physiological response associated with creative processing has been corroborated. In Model 1, we assessed concurrent effects of stress on HPA activation (measured through salivary cortisol), cognitive flexibility, and creativity. In Model 2 and Model 3, the concurrent effects of stress on cognitive flexibility, creativity and SAM activation were investigated. SAM activation was responded to by the activity of dopamine (measured through eye blink rate) and noradrenaline (measured through pupil diameter). Results demonstrated that stress facilitated HPA and SAM activation, which impaired cognitive flexibility, leading to reduced creative performance. Through testing the serial mediation models in this study, a more comprehensive framework was constructed based on the changes in hormones and neurotransmitters under stress.