Research Topic

The Functional Changes in Sensory Ganglion Leading to Pain Hypersensitivity

About this Research Topic

Neuron-glial interaction is considered a critical mechanism involved in the enhancement of TG neuronal excitability. It is also known that macrophages accumulate in the TG following trigeminal nerve injury. Macrophage accumulation occurs in the TG after trigeminal nerve injury. Activated glial cells and macrophages generate and release various molecules, and neuron-glial cell and neuron-macrophage communication occurs. This communication spreads in a wide area of the sensory ganglion, and injured and uninjured primary neurons are further activated, contributing to persistent pain occurrence. The section aims at publishing important basic research, as well as translational and clinical findings in the field of neuron-glial interaction . The scope of the specialty section is broad, covering all scientific topics and techniques of relevance to the field, from molecular and cellular aspects to animal models and humans. Our goal is to provide a comprehensive forum through which quality research can be disseminated to a wide audience.


Keywords: Pain, Sensory Ganglion, Satellite Cell, Macrophage, Primary Neuron


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.

Neuron-glial interaction is considered a critical mechanism involved in the enhancement of TG neuronal excitability. It is also known that macrophages accumulate in the TG following trigeminal nerve injury. Macrophage accumulation occurs in the TG after trigeminal nerve injury. Activated glial cells and macrophages generate and release various molecules, and neuron-glial cell and neuron-macrophage communication occurs. This communication spreads in a wide area of the sensory ganglion, and injured and uninjured primary neurons are further activated, contributing to persistent pain occurrence. The section aims at publishing important basic research, as well as translational and clinical findings in the field of neuron-glial interaction . The scope of the specialty section is broad, covering all scientific topics and techniques of relevance to the field, from molecular and cellular aspects to animal models and humans. Our goal is to provide a comprehensive forum through which quality research can be disseminated to a wide audience.


Keywords: Pain, Sensory Ganglion, Satellite Cell, Macrophage, Primary Neuron


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.

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Submission Deadlines

27 October 2020 Abstract
27 February 2021 Manuscript

Participating Journals

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

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Topic Editors

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Submission Deadlines

27 October 2020 Abstract
27 February 2021 Manuscript

Participating Journals

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

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