Dopaminergic Regulation of Reward System Connectivity Underpins Pain and Emotional Suffering in Migraine.

摘要: Purpose It has been suggested that reward system dysfunction may account for emotion and pain suffering in migraine. However, there is a lack of evidence whether the altered connectivity directly associated with clinical manifestations, including negative affect ictal severity and, at molecular level, dopamine (DA) D2/D3 receptors (D2/3Rs) signaling implicated encoding motivational emotional cues. Patients Methods We acquired resting-state functional MRI from interictal episodic migraine (EM) patients age-matched healthy controls, as well positron emission tomography (PET) [11C]raclopride, selective radiotracer DA D2/3Rs, subset these participants. The nucleus accumbens (NAc) was seeded to measure (FC) D2/3Rs availability based on its essential involvement pain-related aversive/reward functions. Associations brain measures positive/negative were also assessed. Results Compared EM group showed weaker right NAc areas regulation, such amygdala, rostral anterior cingulate cortex, hippocampus, thalamus; but stronger left dorsolateral prefrontal cortex lingual gyrus. Moreover, among connectivities, only NAc-amygdala inversely correlated (diagnostic group-by-D2/3Rs interaction p < 0.007). At lower positive greater over head facial extension area (pain intensity number summation, PAINS). Conclusion Together, our findings suggest connectivity, specifically between might be affected by endogenous signaling, process neural mechanism underlies migraineurs.