Abstract:
:It is known that interleukin-1beta facilitates pain, but the mechanisms of this are not understood. This study investigated the role of interleukin-1beta in the expression of Fos, a marker of neuronal activation, and hyperalgesia caused by injecting complete Freund's adjuvant into one hind paw of the rat. Interleukin-receptor antagonist (interleukin-1ra, 0.005 mg/rat) was given intrathecally twice, 24 h before complete Freund's adjuvant and immediately before complete Freund's adjuvant injection, to block interleukin-1beta action. Fos expression was measured 2 h after complete Freund's adjuvant injection. Paw withdrawal latency was used to assess hyperalgesia. The findings were that interleukin-1ra inhibited inflammation-induced Fos expression and hyperalgesia, which suggests that endogenous interleukin-1beta facilitates transmission of noxious messages at the spinal level by processes involving an enhanced Fos expression.
journal_name
Neuroreportjournal_title
Neuroreportauthors
Li A,Lao L,Wang Y,Zhang H,Ren K,Berman BM,Zhang Rdoi
10.1097/WNR.0b013e3280586839subject
Has Abstractpub_date
2007-03-26 00:00:00pages
495-8issue
5eissn
0959-4965issn
1473-558Xpii
00001756-200703260-00019journal_volume
18pub_type
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