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Journal of Pharmacology And Experimental Therapeutics Fast Forward
First published on April 14, 2005; DOI: 10.1124/jpet.105.084988


0022-3565/05/3141-437-445$20.00
JPET 314:437-445, 2005
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*TETRODOTOXIN

NEUROPHARMACOLOGY

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

Shinki Yoshida, and Shigeji Matsumoto

Department of Physiology, Nippon Dental University, School of Dentistry at Tokyo, Fujimi-cho, Chiyoda-ku, Tokyo, Japan

To determine whether the {alpha}-dendrotoxin ({alpha}-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. {alpha}-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 {alpha}-DTX application increased the number of action potentials without changing the resting membrane potential. Irrespective of the absence and presence of 0.1 µM {alpha}-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 {alpha}-DTX. TEA prolonged the duration of action potentials in the absence or presence of 0.1 µM {alpha}-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 {alpha}-DTX application, 4-AP (0.5 mM) and TEA (2 mM) still regulate the intrinsic firing properties of action potential number and shape.


Received February 15, 2005; accepted April 8, 2005.

Address correspondence to: Shinki Yoshida, Department of Physiology, Nippon Dental University, School of Dentistry at Tokyo, 1-9-20 Fujimi, Chiyoda-ku, Tokyo 102-8159, Japan. E-mail: shinki{at}tokyo.ndu.ac.jp




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X. X. Chi and G. D. Nicol
Manipulation of the Potassium Channel Kv1.1 and Its Effect on Neuronal Excitability in Rat Sensory Neurons
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