Abstract
Advances in the characterization of pain signaling in recent years indicate that distinct neurophysiological and neurochemical mechanisms contribute to pain arising from injury to the nervous system (neuropathic pain). Tissue injury results in the release of pro-nociceptive mediators that sensitize peripheral nerve terminals (peripheral sensitization), leading to neurochemical and phenotypic alterations of sensory neurons and increased excitability of spinal cord dorsal horn neurons (central sensitization). In addition, the response of the nervous system to pain is not static, but is modulated by descending systems originating in the brain that can modulate pain thresholds. In this review, attention is given to the experimental modeling of neuropathic pain in preclinical studies. Recently, an increased understanding of the neurophysiological plasticity of the nervous system in response to chronic pain has led to the discovery and development of novel pharmacological interventions that may have clinical utility in treating neuropathic pain.
Keywords: Neuropathic pain, spinal nerve ligation, chronic constriction injury, diabetic neuropathy, chemotherapy-induced neuropathy
Current Pharmaceutical Design
Title: Neuropathic Pain: Models and Mechanisms
Volume: 15 Issue: 15
Author(s): Janel M. Boyce-Rustay and Michael F. Jarvis
Affiliation:
Keywords: Neuropathic pain, spinal nerve ligation, chronic constriction injury, diabetic neuropathy, chemotherapy-induced neuropathy
Abstract: Advances in the characterization of pain signaling in recent years indicate that distinct neurophysiological and neurochemical mechanisms contribute to pain arising from injury to the nervous system (neuropathic pain). Tissue injury results in the release of pro-nociceptive mediators that sensitize peripheral nerve terminals (peripheral sensitization), leading to neurochemical and phenotypic alterations of sensory neurons and increased excitability of spinal cord dorsal horn neurons (central sensitization). In addition, the response of the nervous system to pain is not static, but is modulated by descending systems originating in the brain that can modulate pain thresholds. In this review, attention is given to the experimental modeling of neuropathic pain in preclinical studies. Recently, an increased understanding of the neurophysiological plasticity of the nervous system in response to chronic pain has led to the discovery and development of novel pharmacological interventions that may have clinical utility in treating neuropathic pain.
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Cite this article as:
Boyce-Rustay M. Janel and Jarvis F. Michael, Neuropathic Pain: Models and Mechanisms, Current Pharmaceutical Design 2009; 15 (15) . https://dx.doi.org/10.2174/138161209788186272
DOI https://dx.doi.org/10.2174/138161209788186272 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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