Research Topic

Role of Glia in Pathological Pain

About this Research Topic

Pathological pain occurs when neurons along the pain signaling pathways are abnormally activated. One key component leading to the development and maintenance of pathological pain is excessive activation of spinal dorsal horn neurons (or spinal central sensitization). Studies over the past two decades have demonstrated that dysfunction of glial cells (mainly microglia and astrocytes) plays a critical role in spinal central sensitization. Glial cells regulate neuronal activity through releasing pro- and anti- inflammatory mediators. Many mediators released from glial cells have been identified in the spinal dorsal horn, such as pro- and anti- inflammatory cytokines, chemokines, BDNF, ROS, glutamate, GABA, D-serine, and ATP. These mediators alter neuronal activities either by modulating glutamatergic or GABAergic synaptic activities, or by directly acting on ligand-gated channels on neurons. Furthermore, glial cells (mainly astrocytes) regulate glutamatergic synaptic activity by re-uptaking glutamate via glial glutamate transporters, and GABAergic synaptic activity by re-uptaking GABA via GABA transporters. Glial glutamate transporters are also implicated in GABA synthesis at presynaptic terminals through the glutamate-glutamine cycle. Functional regulation of glial mediators and transporters has been proven to be effective in controlling aberrant neuronal activity in the spinal dorsal horn and pathological pain. Therefore, identifying signalling molecules regulating the glial neuronal interaction provides immense potential for the development of novel analgesics. In this Research Topic, we welcome original research and review articles promoting discussion on all areas relating but not limited to:
- neuron-glial interactions
- glial activation and proliferation
- synthesis and release of glial mediators
- role of glial glutamate transporters and GABA transporters in pathological pain conditions
- regulation of glial glutamate transporters and GABA transporters
- synaptic plasticity induced by glial mediators or transporters


Keywords: Glial Cells, Spinal Dorsal Horn, Glutamatergic Synaptic Activity, GABAergic Synaptic Activity, Neuron-Glial Interactions


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

Pathological pain occurs when neurons along the pain signaling pathways are abnormally activated. One key component leading to the development and maintenance of pathological pain is excessive activation of spinal dorsal horn neurons (or spinal central sensitization). Studies over the past two decades have demonstrated that dysfunction of glial cells (mainly microglia and astrocytes) plays a critical role in spinal central sensitization. Glial cells regulate neuronal activity through releasing pro- and anti- inflammatory mediators. Many mediators released from glial cells have been identified in the spinal dorsal horn, such as pro- and anti- inflammatory cytokines, chemokines, BDNF, ROS, glutamate, GABA, D-serine, and ATP. These mediators alter neuronal activities either by modulating glutamatergic or GABAergic synaptic activities, or by directly acting on ligand-gated channels on neurons. Furthermore, glial cells (mainly astrocytes) regulate glutamatergic synaptic activity by re-uptaking glutamate via glial glutamate transporters, and GABAergic synaptic activity by re-uptaking GABA via GABA transporters. Glial glutamate transporters are also implicated in GABA synthesis at presynaptic terminals through the glutamate-glutamine cycle. Functional regulation of glial mediators and transporters has been proven to be effective in controlling aberrant neuronal activity in the spinal dorsal horn and pathological pain. Therefore, identifying signalling molecules regulating the glial neuronal interaction provides immense potential for the development of novel analgesics. In this Research Topic, we welcome original research and review articles promoting discussion on all areas relating but not limited to:
- neuron-glial interactions
- glial activation and proliferation
- synthesis and release of glial mediators
- role of glial glutamate transporters and GABA transporters in pathological pain conditions
- regulation of glial glutamate transporters and GABA transporters
- synaptic plasticity induced by glial mediators or transporters


Keywords: Glial Cells, Spinal Dorsal Horn, Glutamatergic Synaptic Activity, GABAergic Synaptic Activity, Neuron-Glial Interactions


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

About Frontiers Research Topics

With their unique mixes of varied contributions from Original Research to Review Articles, Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author.

Topic Editors

Loading..

Submission Deadlines

16 November 2020 Abstract
01 March 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

Loading..

Topic Editors

Loading..

Submission Deadlines

16 November 2020 Abstract
01 March 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

Loading..
Loading..

total views article views article downloads topic views

}
 
Top countries
Top referring sites
Loading..