Authors' present addresses T. Doan: Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA 30322, USA.
Potassium channels Kv1.1, Kv1.2 and Kv1.6 influence excitability of rat visceral sensory neurons
Article first published online: 22 JUL 2004
The Journal of Physiology
Volume 541, Issue 2, pages 467–482, June 2002
How to Cite
Glazebrook, P. A., Ramirez, A. N., Schild, J. H., Shieh, C.-C., Doan, T., Wible, B. A. and Kunze, D. L. (2002), Potassium channels Kv1.1, Kv1.2 and Kv1.6 influence excitability of rat visceral sensory neurons. The Journal of Physiology, 541: 467–482. doi: 10.1113/jphysiol.2001.018333
C.-C. Shieh: Neurological and Urological Diseases Research, Department 47C, Building AP9A, Abbott Laboratories, 100 Abbott Park Road, Abbott Park, IL 60064-6125, USA.
- Issue published online: 22 JUL 2004
- Article first published online: 22 JUL 2004
- (Resubmitted 5 February 2002; accepted 5 March 2002)
Voltage-gated potassium channels, Kv1.1, Kv1.2 and Kv1.6, were identified as PCR products from mRNA prepared from nodose ganglia. Immunocytochemical studies demonstrated expression of the proteins in all neurons from ganglia of neonatal animals (postnatal days 0-3) and in 85-90 % of the neurons from older animals (postnatal days 21-60). In voltage clamp studies, α-dendrotoxin (α-DTX), a toxin with high specificity for these members of the Kv1 family, was used to examine their contribution to K+ currents of the sensory neurons. α-DTX blocked current in both A- and C-type neurons. The current had characteristics of a delayed rectifier with activation positive to −50 mV and little inactivation during 250 ms pulses. In current-clamp experiments α-DTX, used to eliminate the current, had no effect on resting membrane potential and only small effects on the amplitude and duration of the action potential of A- and C-type neurons. However, there were prominent effects on excitability. α-DTX lowered the threshold for initiation of discharge in response to depolarizing current steps, reduced spike after-hyperpolarization and increased the frequency/pattern of discharge of A- and C-type neurons at membrane potentials above threshold. Model simulations were consistent with these experimental results and demonstrated how the other major K+ currents function in response to the loss of the α-DTX-sensitive current to effect these changes in action potential wave shape and discharge.