Effects of PGE(2) on neurons from rat dorsal root ganglia in intact and adjuvant-inflamed rats: role of NGF on PGE(2)-induced depolarization.

Abstract

The effects of prostaglandin E(2) (PGE(2)) on primary afferent neurons were studied by intracellular recording from small (<30 microm) dorsal root ganglion (DRG) neurons cultured for up to 3 days. PGE(2) (10(-9)-10(-5) M) depolarized 4-10% of neurons cultured with nerve growth factor (NGF) in intact rats. The percentage of neurons depolarized increased in a concentration dependent manner, while the average amplitude of the depolarization did not change with concentration. The threshold to evoke an action potential was decreased by PGE(2) (10(-9)-10(-5) M) with the maximum percentage at 10(-9) M, and this effect was also observed in neurons not depolarized by PGE(2). Whether a neuron was depolarized by PGE(2) was not related with its capsaicin (CAP) sensitivity. In addition, we examined whether NGF influences the PGE(2) response of neurons in adjuvant-inflamed young adult animals. Removal of NGF from culture medium did not change the percentage of neurons depolarized by PGE(2) in intact rats (20 and 18% for neurons cultured without or with NGF for 2-3 days, respectively). Adjuvant induced inflammation increased the percentage of neurons depolarized by PGE(2) to 38%, but this was not reversed by an addition of anti-NGF antibody to the culture medium, suggesting that NGF does not play a substantial role in the increase in sensitivity to be depolarized by PGE(2).