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Published on: January 18, 2019
Microglia and spinal cord synaptic plasticity in persistent pain
Sarah Taves1, Temugin Berta, Gang Chen
1Pain Signaling and Plasticity Laboratory, Department of Anesthesiology, Duke University Medical Center, Durham, NC 27710, USA.
Abstract:
Microglia are regarded as macrophages in the central nervous system (CNS) and play an important role in neuroinflammation in the CNS. Microglial activation has been strongly implicated in neurodegeneration in the brain. Increasing evidence also suggests an important role of spinal cord microglia in the genesis of persistent pain, by releasing the proinflammatory cytokines tumor necrosis factor-alpha (TNFα), Interleukine-1beta (IL-1β), and brain derived neurotrophic factor (BDNF). In this review, we discuss the recent findings illustrating the importance of microglial mediators in regulating synaptic plasticity of the excitatory and inhibitory pain circuits in the spinal cord, leading to enhanced pain states. Insights into microglial-neuronal interactions in the spinal cord dorsal horn will not only further our understanding of neural plasticity but may also lead to novel therapeutics for chronic pain management.
Insights
Spinal cord microglia contribute to persistent pain by releasing inflammatory mediators that alter synaptic plasticity. Understanding these microglial-neuronal interactions may lead to new chronic pain treatments.
Area of Science:
- Neuroscience
- Immunology
Background:
- Microglia are central nervous system (CNS) macrophages involved in neuroinflammation.
- Microglial activation is linked to neurodegeneration and persistent pain.
- Spinal cord microglia release pro-inflammatory cytokines like TNFα, IL-1β, and BDNF, contributing to pain sensitization.
Purpose of the Study:
- To review recent findings on the role of microglial mediators in spinal cord synaptic plasticity.
- To explore microglial-neuronal interactions in the dorsal horn relevant to pain circuits.
- To highlight the therapeutic potential of targeting microglial activity for chronic pain management.
Main Methods:
- Review of current scientific literature on microglia, neuroinflammation, and pain.
- Analysis of studies investigating microglial mediators and their effects on synaptic plasticity.
- Examination of research on microglial-neuronal communication in the spinal cord dorsal horn.
Main Results:
- Microglial mediators significantly regulate synaptic plasticity in spinal cord pain circuits.
- Activation of spinal cord microglia enhances excitatory and inhibitory pain signaling.
- Microglial-neuronal interactions in the dorsal horn are crucial for maintaining chronic pain states.
Conclusions:
- Spinal cord microglia play a critical role in the development and maintenance of persistent pain.
- Targeting microglial mediators and their interactions with neurons offers a promising avenue for novel pain therapeutics.
- Further research into microglial functions in the CNS can advance our understanding of neural plasticity and pain management.
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