TY - JOUR
T1 - Changes in c-fos induction in dorsal horn neurons by hindpaw formalin stimulation following tibial neurotomy
AU - Sugimoto, Tomosada
AU - Ichikawa, Hiroyuki
AU - Mitani, Seiji
AU - Hitsu, Akemi
AU - Tadao, Nakago
N1 - Copyright:
Copyright 2014 Elsevier B.V., All rights reserved.
PY - 1994/4/11
Y1 - 1994/4/11
N2 - The hindpaw was partially denervated by the tibial nerve transection in adult rats. At post-transection intervals varying from 2 to 168 days, the hindpaw was stimulated bilaterally by subcutaneous injection of formalin. The excitability of dorsal horn neurons was expressed as the percentage ratio of the number of formalin-induced c-fos protein-like immunoreactive neurons (fos-neurons) on the neurotomized (experimental) side to that on the un-neurotomized (control) side. At 2 days post-injury, a marked reduction in the number of fos-neurons was noted in laminae I-VII of the lumbar spinal cord. Among these, reduction was greatest in the medial 3 8 of laminae I and II (terminal field of the tibial nerve, i.e. tibial territory), and smallest in the lateral 5 8 of the same laminae (the peroneal/hip territory). The low level of c-fos induction remained unchanged for 7 days. At 14 days, the excitability of neurons in all laminae showed a marked increase compared to the post-injury days 2 and 3 combined. Thereafter, the increased level of excitability in the tibial territory was maintained throughout the post-injury period examined in this study. On the other hand, a statistically significant increase in excitability in the peroneal/hip territory was only seen between 14 and 28 days and the excitability almost returned to the baseline (2 days and 3 post-transection combined) level at 42 days. Although deeper laminae (III-VII) contained much less formalin-induced fos-neurons, they also exhibited post-injury excitability changes with a temporal pattern similar to that of the peroneal/hip territory of laminae I and II. Possible mechanisms underlying the post-injury hypersensitivity are discussed in the light of peripheral and central changes following peripheral nerve injuries.
AB - The hindpaw was partially denervated by the tibial nerve transection in adult rats. At post-transection intervals varying from 2 to 168 days, the hindpaw was stimulated bilaterally by subcutaneous injection of formalin. The excitability of dorsal horn neurons was expressed as the percentage ratio of the number of formalin-induced c-fos protein-like immunoreactive neurons (fos-neurons) on the neurotomized (experimental) side to that on the un-neurotomized (control) side. At 2 days post-injury, a marked reduction in the number of fos-neurons was noted in laminae I-VII of the lumbar spinal cord. Among these, reduction was greatest in the medial 3 8 of laminae I and II (terminal field of the tibial nerve, i.e. tibial territory), and smallest in the lateral 5 8 of the same laminae (the peroneal/hip territory). The low level of c-fos induction remained unchanged for 7 days. At 14 days, the excitability of neurons in all laminae showed a marked increase compared to the post-injury days 2 and 3 combined. Thereafter, the increased level of excitability in the tibial territory was maintained throughout the post-injury period examined in this study. On the other hand, a statistically significant increase in excitability in the peroneal/hip territory was only seen between 14 and 28 days and the excitability almost returned to the baseline (2 days and 3 post-transection combined) level at 42 days. Although deeper laminae (III-VII) contained much less formalin-induced fos-neurons, they also exhibited post-injury excitability changes with a temporal pattern similar to that of the peroneal/hip territory of laminae I and II. Possible mechanisms underlying the post-injury hypersensitivity are discussed in the light of peripheral and central changes following peripheral nerve injuries.
KW - Dorsal horn
KW - Peripheral nerve injury
KW - Peroneal nerve
KW - Somatotopy
KW - Tibial nerve
KW - c-fos
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U2 - 10.1016/0006-8993(94)90942-3
DO - 10.1016/0006-8993(94)90942-3
M3 - Article
C2 - 8032900
AN - SCOPUS:0028205893
VL - 642
SP - 348
EP - 354
JO - Molecular Brain Research
JF - Molecular Brain Research
SN - 0006-8993
IS - 1-2
ER -