The nervous system is a major system in the body that is the master of control and communication in and throughout the body (Marieb and Hoehn 345) There are two parts of the nervous system, the central nervous system, which consists of the brain and the spinal cord, and the peripheral nervous system, which is everything outside of the brain and the spinal cord. The peripheral nervous system deals extensively with sensations of the body and these sensations are sent to the central nervous system for interpretation (Marieb and Hoehn 346). Neuroglia, or glial cells, are supporting cells of the nervous system. Satellite cells are a type of neuroglia in the peripheral nervous system that surround neuron cell bodies (Marieb and Hoehn 348) These cells
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Hyperexcitability, characterized by an increased frequency of unplanned activity and a reduced activation threshold by peripheral stimuli, which result in hyperalgesia and allodynia phenomena seen after injury, is caused by changes in properties of the pericardium. Based on studies on rodents, inflammation or constriction indicates that nerve injury not only induces changes in neurons but also in sensory ganglia satellite cells. Under normal conditions, glial cells are spectators of the nociceptive process, but after peripheral injury, they react displaying morphological changes and releasing glial mediators. Since neurons are the target, the changes seen in the satellite cells involve activation signaling mechanisms between neurons and the glial cells. These changes take place due to increased firing that is produced after the nerve injury. The spontaneous activity associated with the blocking of neuronal activity prevents the development of pain associated with non-physiological behavior. A reduction in the behavioral signs of pain was seen in animals that had two action potential blockers that were administered to mice in an experiment. In this experiment, the action potential blockers prevented the unplanned activity in the injured nerve, before and after the mice were exposed to nerve injury. Also from this experiment, it was found that the activation of satellite cells after the nerve injury is prevented by a local nerved conduction blockade. There is a reduction in the satellite cell activation. Studies show that satellite cells endure profound changes in response to nerve injury. These changes are caused by an increased expression of glial fibrillary acidic protein, decreased expression and sensitivity to potassium channels, increased satellite cell coupling by gap junctions, increased sensitivity to ATP, and the release of ATP and
Hyperexcitability, characterized by an increased frequency of unplanned activity and a reduced activation threshold by peripheral stimuli, which result in hyperalgesia and allodynia phenomena seen after injury, is caused by changes in properties of the pericardium. Based on studies on rodents, inflammation or constriction indicates that nerve injury not only induces changes in neurons but also in sensory ganglia satellite cells. Under normal conditions, glial cells are spectators of the nociceptive process, but after peripheral injury, they react displaying morphological changes and releasing glial mediators. Since neurons are the target, the changes seen in the satellite cells involve activation signaling mechanisms between neurons and the glial cells. These changes take place due to increased firing that is produced after the nerve injury. The spontaneous activity associated with the blocking of neuronal activity prevents the development of pain associated with non-physiological behavior. A reduction in the behavioral signs of pain was seen in animals that had two action potential blockers that were administered to mice in an experiment. In this experiment, the action potential blockers prevented the unplanned activity in the injured nerve, before and after the mice were exposed to nerve injury. Also from this experiment, it was found that the activation of satellite cells after the nerve injury is prevented by a local nerved conduction blockade. There is a reduction in the satellite cell activation. Studies show that satellite cells endure profound changes in response to nerve injury. These changes are caused by an increased expression of glial fibrillary acidic protein, decreased expression and sensitivity to potassium channels, increased satellite cell coupling by gap junctions, increased sensitivity to ATP, and the release of ATP and