Abstract
Neuropathic pain and phantom phenomena occur commonly after spinal cord injury (SCI) but their molecular basis is not yet fully understood. Recent findings demonstrate abnormal expression of the Nav1.3 Na(+) channel within second-order spinal cord dorsal horn neurons and third-order thalamic neurons along the pain pathway after SCI, and suggest that this change makes these neurons hyperexcitable so that they act as pain amplifiers and generators. Delineation of molecular changes that contribute to hyperexcitability of pain-signaling neurons might lead to identification of molecular targets that will be useful in the treatment of neuropathic pain after SCI and related nervous system injuries.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Humans
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NAV1.3 Voltage-Gated Sodium Channel
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Nerve Tissue Proteins / metabolism*
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Neural Pathways / cytology
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Neural Pathways / metabolism*
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Neurons / metabolism
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Pain / etiology
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Pain / metabolism*
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Pain / physiopathology
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Phantom Limb / etiology*
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Phantom Limb / metabolism
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Phantom Limb / physiopathology
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Posterior Horn Cells / metabolism
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Rats
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Sodium Channels / metabolism*
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Spinal Cord Injuries / complications*
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Spinal Cord Injuries / metabolism*
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Spinal Cord Injuries / physiopathology
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Thalamus / cytology
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Thalamus / metabolism*
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Up-Regulation
Substances
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NAV1.3 Voltage-Gated Sodium Channel
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Nerve Tissue Proteins
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SCN3A protein, human
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Sodium Channels