1: Eur Spine J. 2002 Oct;11(5):467-75. Epub 2002 Jun 04. 

Dorsal root sensitivity to interleukin-1 beta, interleukin-6 and tumor necrosis
factor in rats.

Ozaktay AC, Cavanaugh JM, Asik I, DeLeo JA, Weinstein JN.

Wayne State University, Bioengineering Center, 818W Hancock, Detroit, MI 48201,
USA. ozaktay@wayne.edu

The release of inflammatory cytokines caused by a disrupted disc may play a
critical role in pain production at nerve endings, axons, and nerve cell bodies.
Herniated disc tissue has been shown to release inflammatory cytokines such as
interleukin-1 beta (IL-1beta), interleukin-6 (IL-6), tumor necrosis factor
(TNF), and other algesic chemicals. This study was designed to characterize the
effects of these proinflammatory cytokines on the somatosensory neural response
at the dorsal root level in rats. It is hypothesized that their effects on nerve
endings in disc and adjacent tissue contribute to low-back pain, and the effects
on dorsal root axons and ganglia contribute to radiculopathy and sciatica.
Surgically isolated sacral dorsal roots were investigated by electrophysiologic
techniques. IL-1beta, IL-6, or TNF (100 ng, each) were applied onto the dorsal
roots. Neural responses and mechanosensitivity of the receptive fields were
evaluated over time. The results showed that 3 h after each cytokine
application, the neural activity was statistically decreased. The mechanical
sensitivity of the receptive fields increased at 90 min following IL-1beta or
TNF application, and returned to normal more than 3 h after IL-1beta
application. IL-1beta, IL-6, and TNF may be neurotoxic to dorsal root axons.
Furthermore IL-1beta and TNF may sensitize the peripheral receptive fields. This
study suggests that dorsal roots may be impaired by these proinflammatory
cytokines.

PMID: 12384756 [PubMed - indexed for MEDLINE]