RT Journal Article SR Electronic T1 Effects of α-Dendrotoxin on K+ Currents and Action Potentials in Tetrodotoxin-Resistant Adult Rat Trigeminal Ganglion Neurons JF Journal of Pharmacology and Experimental Therapeutics JO J Pharmacol Exp Ther FD American Society for Pharmacology and Experimental Therapeutics SP 437 OP 445 DO 10.1124/jpet.105.084988 VO 314 IS 1 A1 Shinki Yoshida A1 Shigeji Matsumoto YR 2005 UL http://jpet.aspetjournals.org/content/314/1/437.abstract AB To determine whether the α-dendrotoxin (α-DTX)-sensitive current [D current, slow inactivating transient current (ID)] contributes to the modification of neuronal function in small-diameter adult rat trigeminal ganglion (TG) neurons insensitive to 1 μM tetrodotoxin (TTX), we performed two different types of experiments. In the voltage-clamp mode, two distinct K+ current components, a fast inactivating transient current (IA) and a dominant sustained current (IK), were identified. α-DTX (0.1 μM), ranging from 0.001 to 1 μM, maximally decreased IA by approximately 20% and IK by approximately 16.1% at a +50-mV step pulse, and 0.1 μM α-DTX application increased the number of action potentials without changing the resting membrane potential. Irrespective of the absence and presence of 0.1 μM α-DTX, applications of 4-aminopyridine (4-AP; 0.5 mM) and tetraethylammonium (TEA; 2 mM) inhibited approximately 50% inhibition of IA and IK, 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 μM α-DTX. TEA prolonged the duration of action potentials in the absence or presence of 0.1 μM α-DTX. These results suggest that ID contributes to the modification of neuronal function in adult rat TTX-resistant TG neurons, but after the loss of ID due to 0.1 μM α-DTX application, 4-AP (0.5 mM) and TEA (2 mM) still regulate the intrinsic firing properties of action potential number and shape. The American Society for Pharmacology and Experimental Therapeutics