Effects of α-Dendrotoxin on K+ Currents and Action Potentials in Tetrodotoxin-Resistant Adult Rat Trigeminal Ganglion Neurons

Abstract

To determine whether the alpha-dendrotoxin (alpha-DTX)-sensitive current [D current, slow inactivating transient current (I(D))] contributes to the modification of neuronal function in small-diameter adult rat trigeminal ganglion (TG) neurons insensitive to 1 microM tetrodotoxin (TTX), we performed two different types of experiments. In the voltage-clamp mode, two distinct K+ current components, a fast inactivating transient current (I(A)) and a dominant sustained current (I(K)), were identified. Alpha-DTX (0.1 microM), ranging from 0.001 to 1 microM, maximally decreased I(A) by approximately 20% and I(K) by approximately 16.1% at a +50-mV step pulse, and 0.1 microM alpha-DTX application increased the number of action potentials without changing the resting membrane potential. Irrespective of the absence and presence of 0.1 microM alpha-DTX, applications of 4-aminopyridine (4-AP; 0.5 mM) and tetraethylammonium (TEA; 2 mM) inhibited approximately 50% inhibition of I(A) and I(K), respectively. 4-AP (0.5 mM) depolarized the resting membrane potential and increased the number of action potentials in the absence or presence of 0.1 microM alpha-DTX. TEA prolonged the duration of action potentials in the absence or presence of 0.1 microM alpha-DTX. These results suggest that I(D) contributes to the modification of neuronal function in adult rat TTX-resistant TG neurons, but after the loss of I(D) due to 0.1 microM alpha-DTX application, 4-AP (0.5 mM) and TEA (2 mM) still regulate the intrinsic firing properties of action potential number and shape.