Microglial-derived nitric oxide regulates amygdala synaptic plasticity to drive chronic pain and depression induced by lumbar disc herniation
By Admin | June 02, 2025
Introduction
Low back pain is a leading cause of disability worldwide, with high prevalence and a substantial socioeconomic impact (Hartvigsen et al., 2018). Lumbar disc herniation (LDH) is recognized as a major cause of low back pain, often resulting in chronic radicular pain and neuropathic symptoms (Kreiner et al., 2014). Beyond nociceptive symptoms, patients with LDH frequently exhibit affective comorbidities, such as depression, which substantially worsen prognosis and complicate treatment (Martucci and Mackey, 2018). While peripheral and spinal mechanisms of LDH-associated pain have been extensively studied, the supraspinal processes that integrate nociceptive and emotional dimensions of LDH remain poorly understood.
LDH typically involves the displacement of disc material beyond intervertebral boundaries, resulting in nerve root irritation and inflammation. However, these mechanisms inadequately explain the psychosomatic manifestations observed
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