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Abnormal substance P release from the spinal cord following injury to primary sensory neurons
Author(s) -
Malcangio Marzia,
Ramer Matt S.,
Jones Martyn G.,
McMahon Stephen B.
Publication year - 2000
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2000.00946.x
Subject(s) - axotomy , spinal cord , substance p , nociception , sciatic nerve , lesion , medicine , anatomy , neuropathic pain , spinal cord injury , neuropeptide , peripheral nerve injury , nerve injury , sensory system , central nervous system , chemistry , neuroscience , anesthesia , biology , pathology , receptor
The neuropeptide substance P (SP) modulates nociceptive transmission within the spinal cord. Normally, SP is uniquely contained in a subpopulation of small‐calibre axons (Aδ‐ and C‐fibres) within primary afferent nerve. However, it has been shown that after nerve transection, besides being downregulated in small axons, SP is expressed de novo in large myelinated Aβ‐fibres. In this study we investigated whether, following peripheral nerve injury, SP was released de novo from the spinal cord after selective activation of Aβ‐fibres. Spinal cords with dorsal roots attached were isolated in vitro from rats 2 weeks following distal sciatic axotomy or proximal spinal nerve lesion (SNL). The ipsilateral dorsal roots were electrically stimulated for two consecutive periods at low‐ or high‐threshold fibre strength, spinal cord superfusates were collected and SP content was determined by radioimmunoassay. SNL, but not axotomized or control rat cords, released significant amounts of SP after selective activation of Aβ‐fibres. Not only do these data support the idea that Aβ myelinated fibres contribute to neuropathic pain by releasing SP, they also illustrate the importance of the proximity of the lesion to the cell body.