We examined the effects of α
2-adrenergic agonist, dexmedetomidine(DEX), on tetrodotoxin-resistant (TTX-r) Na
+ currents using small-sized dorsal root ganglion(DRG) cells of the rats. Whole cell patch-clamp configuration was used. After control Na
+ current was recorded, DEX was added to the extracellular solution. Yohimbine and prazosin were used to differentiate the contribution of α
2-adrenergic receptor from that of α
1-adrenergic receptor. The peak TTX-r Na
+ currents were significantly and dose dependently inhibited by DEX(p<0.05). Yohimbine attenuated the suppressive effects of DEX on TTX-r Na
+ currents, while prazosin did not alter the effects of DEX. Thus, DEX inhibited TTX-r Na
+ currents by way of α
2-adrenergic receptors but not α
1-adrenergic receptors. Therefore, it is suggested that DEX has an inhibitory effect on TTX-r Na
+ channels through α
2-adrenergic receptors.
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