Inflammatory Changes in Paravertebral Sympathetic Ganglia in Two Rat Pain Models / 神经科学通报·英文版
Neuroscience Bulletin
;
(6): 85-97, 2018.
Article
in English
| WPRIM
| ID: wpr-777073
ABSTRACT
Injury to peripheral nerves can lead to neuropathic pain, along with well-studied effects on sensory neurons, including hyperexcitability, abnormal spontaneous activity, and neuroinflammation in the sensory ganglia. Neuropathic pain can be enhanced by sympathetic activity. Peripheral nerve injury may also damage sympathetic axons or expose them to an inflammatory environment. In this study, we examined the lumbar sympathetic ganglion responses to two rat pain models ligation of the L5 spinal nerve, and local inflammation of the L5 dorsal root ganglion (DRG), which does not involve axotomy. Both models resulted in neuroinflammatory changes in the sympathetic ganglia, as indicated by macrophage responses, satellite glia activation, and increased numbers of T cells, along with very modest increases in sympathetic neuron excitability (but not spontaneous activity) measured in ex vivo recordings. The spinal nerve ligation model generally caused larger responses than DRG inflammation. Plasticity of the sympathetic system should be recognized in studies of sympathetic effects on pain.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Pain
/
Pathology
/
Physiology
/
Action Potentials
/
Receptors, Antigen, T-Cell, alpha-beta
/
Rats, Sprague-Dawley
/
Patch-Clamp Techniques
/
Neurogenic Inflammation
/
Disease Models, Animal
/
Peripheral Nerve Injuries
Limits:
Animals
Language:
English
Journal:
Neuroscience Bulletin
Year:
2018
Type:
Article
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