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THE RESPONSE OF SATELLITE GLIAL CELLS TO P2X7 RECEPTOR ACTIVATION
- Date Issued:
- 2017
- Abstract/Description:
- Satellite glial cells (SGCs) surround the cell bodies of neurons of the peripheral nervous system, including those of the sensory ganglia. Their close apposition to the neuronal soma allows for bi-directional communication between neurons and SGCs, which are thought to regulate neuronal activity. After nerve injury, SGCs in the dorsal root ganglia contribute to neuropathic pain. Although the mechanisms are not fully understood, SGCs show increased coupling via gap junctions, and communicate with the neuron via bi-directional purinergic signaling after nerve injury. The increased coupling between SGCs and neurons may have implications for chronic pain following peripheral nerve injury. In vivo studies suggest that injury through the administration of capsaicin to the sensory nerve endings causes SGCs to be activated and proliferate. We have shown that capsaicin treatment in an in vitro co-culture of sensory neurons and SGCs increased the expression of the proliferation marker, Ki-67 in the glia. Here, we examine whether purinergic signaling plays a role in the promotion of SGC proliferation.
Title: | THE RESPONSE OF SATELLITE GLIAL CELLS TO P2X7 RECEPTOR ACTIVATION. |
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Name(s): |
Kursewicz, Christina D, Author Lambert,Stephen, Committee Chair University of Central Florida, Degree Grantor |
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Type of Resource: | text | |
Date Issued: | 2017 | |
Publisher: | University of Central Florida | |
Language(s): | English | |
Abstract/Description: | Satellite glial cells (SGCs) surround the cell bodies of neurons of the peripheral nervous system, including those of the sensory ganglia. Their close apposition to the neuronal soma allows for bi-directional communication between neurons and SGCs, which are thought to regulate neuronal activity. After nerve injury, SGCs in the dorsal root ganglia contribute to neuropathic pain. Although the mechanisms are not fully understood, SGCs show increased coupling via gap junctions, and communicate with the neuron via bi-directional purinergic signaling after nerve injury. The increased coupling between SGCs and neurons may have implications for chronic pain following peripheral nerve injury. In vivo studies suggest that injury through the administration of capsaicin to the sensory nerve endings causes SGCs to be activated and proliferate. We have shown that capsaicin treatment in an in vitro co-culture of sensory neurons and SGCs increased the expression of the proliferation marker, Ki-67 in the glia. Here, we examine whether purinergic signaling plays a role in the promotion of SGC proliferation. | |
Identifier: | CFH2000172 (IID), ucf:45960 (fedora) | |
Note(s): |
2017-05-01 B.S. College of Medicine, Bachelors This record was generated from author submitted information. |
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Subject(s): |
satellite glial cells purinergic signaling P2X7 proliferation BzATP |
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Persistent Link to This Record: | http://purl.flvc.org/ucf/fd/CFH2000172 | |
Restrictions on Access: | campus 2020-05-01 | |
Host Institution: | UCF |