Ann Med Med Res | Volume 8, Issue 1 | Research Article | Open Access

Neuroinflammation and Synaptic Plasticity: New Insights into Postoperative Pain Mechanism

Chengcheng Song*

*Correspondance to: Chengcheng Song 

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Abstract

Postoperative pain, a common consequence of surgical procedures, is primarily attributed to tissue trauma and the ensuing inflammatory response. This response involves the release of inflammatory mediators such as prostaglandins, cytokines (IL-1β, TNF-α, IL-6), and chemokines, which sensitize nociceptors, enhancing pain perception. Although microglia are the main immune cells in the central nervous system, they play an important role in chronic pain by releasing pro-inflammatory cytokines and regulating synaptic transmission and plasticity, but their specific role in postoperative pain is still unclear. This study investigates synaptic changes and the expression of synaptic proteins like PSD-95 following incision surgery to identify potential therapeutic targets for pain management. Our findings reveal that the upregulation of cytokine IL-6 and TNF-α was activated microglia in the spinal cord, highlighting the neuroinflammation in regulating pain in incision pain model. We also studied PSD-95, a scaffolding protein essential for synaptic function and plasticity, is implicated in central sensitization and neuropathic pain. By evaluating synaptic plasticity and inflammatory reaction, we aim to clarify the neurobiological mechanisms behind pain-related cognitive and emotional disorders and potentially guide future pain treatment strategies. These insights emphasize the complex relationship between synaptic changes and pain-related changes in the central nervous system.

Keywords:

Pain; Post-operative pain; Microglia; PSD-95; Synaptic function

Citation:

Tianjin Medical University, Anshan St, Tianjin, China.

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