Migraine, a neurological disorder characterized by recurring, intense headaches, disproportionately affects a significant portion of the population, particularly females. While its precise etiology remains elusive, it is thought to have arisen from a combination of genetic predisposition and environmental factors. This research endeavors to explore the neurobiological underpinnings of both the sensory and emotional aspects of migraine pain, as well as the associated social impairments. Using the nitroglycerin (NTG) migraine model, which induces vasodilation via systemic administration, we simulated migraine-like symptoms. NTG exposure elicited social deficits in male and female mice. Interestingly, our investigation revealed that Ro 64-6198, a NOP receptor agonist, mitigated NTG-induced migraine-like symptoms, including mechanical allodynia. Conversely, the NOP antagonist SB-612111 blocked the effects of the agonist. In a study assessing sociability under migraine conditions, Ro 64-6198 ameliorated the social dysfunction induced by NTG, while SB-612111 partially attenuated the effects of the NOP agonist. Our neuroanatomical analysis using TRAP2/Ai9 mice, which enable the identification of activated cells and brain regions, demonstrated that NTG treatment markedly heightened activation in various brain regions pertinent to migraine pain and social behavior compared to vehicle-treated subjects. Moreover, these findings suggest that the activation of NOP receptors modulates neuronal activity in specific brain regions involved in migraine pain and social behavior. Our brain-wide analysis will provide us with ample information to better understand the relation between the NOP receptor system and sociability under migraine pain.