A rapid capsaicin-activated current in rat trigeminal ganglion neurons.

Abstract

A subpopulation of pain fibers are activated by capsaicin, the ingredient in red peppers that produces a burning sensation when eaten or placed on skin. Previous studies on dorsal root ganglion neurons indicated that capsaicin activates sensory nerves via a single slowly activating and inactivating inward current. In rat trigeminal neurons, we identified a second capsaicin-activated inward current. This current can be distinguished from the slow one in that it rapidly activates and inactivates, requires Ca2+ for activation, and is insensitive to the potent capsaicin agonist resiniferatoxin. The rapid current, like the slower one, is inhibited by ruthenium red and capsazepine. The two capsaicin-activated inward currents share many similarities with the two inward currents activated by lowering the pH to 6.0. These similarities include kinetics, reversal potentials, responses to Ca2+, and inhibition by ruthenium red and capsazepine. These results suggest that acidic stimuli may be an endogenous activator of capsaicin-gated currents and therefore may rationalize why pain is produced when the plasma acidity is increased, as occurs during ischemia and inflammation.