Abstract
The hyperexcitability of spinal dorsal horn neurons that enhances nociceptive transmission is involved in chronic central neuropathic pain, which develops following traumatic spinal cord injury (SCI). While the generation of neuronal hyperexcitability depends on nociceptive synaptic transmission, recent studies demonstrated that SCI causes persistent glial activation with concomitant neuronal hyperexcitability, thus providing the substrate for central neuropathic pain. When activated by SCI, glial cells undergo morphological and functional changes, causing maladaptive synaptic plasticity in the spinal cord. Activated glial cells increase intracellular and extracellular levels of various sensitizing agents, such as glutamate and proinflammatory cytokines, which enhance nociceptive transmission. In addition, glial cells cause neurons to overexpress ligand-based receptors and ion channels via activation of intracellular signaling events, which maintain chronic neuropathic pain. In this chapter, we describe how activated glial cells contribute to the maintenance of chronic neuropathic pain via neuronal-glial interactions following SCI.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
