Characteristics and consequences of subcellular calcium signalling in spinal neurons and glia in chronic inflammatory and neuropathic pain (A05)

活性诱导的细胞内钙信号在控制中枢神经系统持续适应的过程中起着非常重要的作用。事实上，脊髓神经元、星形胶质细胞和小胶质细胞中的钙信号与适应不良的疼痛可塑性密切相关。在这项研究中，我们将研究突触活动触发的钙信号在脊髓神经胶质网络中不同亚细胞区的时空特征，确定它们在慢性疼痛中是否以及如何改变，并探讨核钙信号如何在持续性疼痛模型中对结构可塑性和伤害性超敏的发展和维持起作用。

Activity-induced intracellular Ca2+ signaling plays an invaluable role in processes that control persistent adaptations within the CNS. Indeed, Ca2+ signaling in spinal cord neurons, astrocytes, and microglia is strongly implicated in maladaptive pain plasticity. In this study, we will investigate the spatiotemporal features of synaptic activity-triggered Ca2+ signals in distinct subcellular compartments within spinal neuroglial networks, determine whether and how they are altered in chronic pain, and investigate how nuclear Ca2+ signals contribute to the development and maintenance of structural plasticity and nociceptive hypersensitivity in persistent pain models.