The article examines the transition from chronic pain to depression through neurogenesis-driven remodeling of microglial cells in the dentate gyrus of the hippocampus. Chronic pain induced by peripheral nerve injury activates microglial cells in the hippocampus, leading to delayed onset of depressive symptoms after 4–8 weeks. These cells increase TNF-α expression more than 2-fold in the hippocampus, medial prefrontal cortex, and amygdala, promoting neuroinflammation and suppressing neurogenesis. Activated microglial cells disrupt the formation of new neurons and synaptic plasticity in the dentate gyrus. IL4-influenced microglial cells, on the other hand, promote neurogenesis through BDNF, thereby increasing resistance to chronic stress and depression. Toll-like receptors (TLR4, TLR5) and NLRP3 in microglial cells regulate neurogenesis and contribute to the pathogenesis of depression. Remodelácia mikrogliálnych buniek tak spája chronickú bolesť s depresiou cez zmeny v hipokampálnej neurogenéze.[1][2][3]