Tumor necrosis factor alpha and interleukin-1beta stimulate the expression of cyclooxygenase II but do not alter prostaglandin E2 receptor mRNA levels in cultured dorsal root ganglia cells.

Tumor necrosis factor alpha (TNFalpha) and interleukin 1beta (IL-1beta) are pro-inflammatory cytokines capable of altering the sensitivity of sensory neurons. Because sensitization elicited by IL-1beta and TNFalpha is blocked by inhibition of the inducible enzyme, cyclooxygenase-II (COX-2), we examined whether these cytokines could increase COX-2 expression in dorsal root ganglion (DRG) cultures. Treatment of cell cultures with either IL-1beta or TNFalpha increases immunoreactive COX-2, as measured by immunoblotting, in a time- and concentration-dependent manner.

Isolation and culture of sensory neurons from the dorsal-root ganglia of embryonic or adult rats.

There is increasing use of isolated sensory neuronal preparations to examine the cellular mechanisms involved in pain signaling. Indeed, these in viro preparations have several advantages that make them beneficial for examining physiological and/or pathological processes affecting neuronal function. With isolated cells it can be determined whether various inflammatory mediators and algogenic agents have direct actions on sensory neurons.