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Peripheral nerve injury induces trans‐synaptic modification of channels, receptors and signal pathways in rat dorsal spinal cord
Author(s) -
Yang Liang,
Zhang FangXiong,
Huang Fen,
Lu YinJing,
Li GuoDong,
Bao Lan,
Xiao HuaSheng,
Zhang Xu
Publication year - 2004
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 - 10.1111/j.0953-816x.2004.03121.x
Subject(s) - dorsal root ganglion , peripheral nerve injury , spinal cord , axotomy , biology , neuropathic pain , nicotinic acetylcholine receptor , nerve injury , neuroscience , postsynaptic potential , nicotinic agonist , acetylcholine receptor , receptor , microbiology and biotechnology , central nervous system , anatomy , sciatic nerve , biochemistry
Peripheral tissue injury‐induced central sensitization may result from the altered biochemical properties of spinal dorsal horn. However, peripheral nerve injury‐induced modification of genes in the dorsal horn remains largely unknown. Here we identified strong changes of 14 channels, 25 receptors and 42 signal transduction related molecules in Sprague–Dawley rat dorsal spinal cord 14 days after peripheral axotomy by cDNA microarray. Twenty‐nine genes were further confirmed by semiquantitative RT‐PCR, Northern blotting, in situ hybridization and immunohistochemistry. These regulated genes included Ca 2+ channel α1E and α2/δ1 subunits, α subunits for Na + channel 1 and 6, Na + channel β subunit, AMAP receptor GluR3 and 4, GABA A receptor α5 subunit, nicotinic acetylcholine receptor α5 and β2 subunits, PKC α, βI and δ isozymes, JNK1–3, ERK2–3, p38 MAPK and BatK and Lyn tyrosine‐protein kinases, indicating that several signal transduction pathways were activated in dorsal spinal cord by peripheral nerve injury. These results demonstrate that peripheral nerve injury causes phenotypic changes in spinal dorsal horn. Increases in Ca 2+ channel α2/δ1 subunit, GABA A receptor α5 subunit, Na + channels and nicotinic acetylcholine receptors in both dorsal spinal cord and dorsal root ganglia indicate their potential roles in neuropathic pain control.