J Physiol Society Meetings
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Physiol Vol 389 pp 629-645
Copyright © 1987 by The Physiological Society
This Article
Right arrow Full Text (PDF)
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Higashi, H
Right arrow Articles by North, R A
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Higashi, H
Right arrow Articles by North, R A

Ouabain augments calcium-dependent potassium conductance in visceral primary afferent neurones of the rabbit.

H Higashi, Y Katayama, K Morita and R A North

Department of Autonomic Physiology, Tokyo Medical and Dental University, Japan.

1. The effects of ouabain (1 nM-100 microM) on the membrane properties of rabbit visceral primary afferent neurones (nodose ganglion cells) were studied with intracellular recordings and voltage-clamp techniques in vitro. 2. Ouabain (greater than or equal to 1 microM) often produced a membrane hyperpolarization associated with a fall of membrane resistance in type C neurones. The ouabain-induced hyperpolarization reversed in polarity at about -90 mV. These suggest that the ouabain-induced hyperpolarization is due to an increase in potassium conductance. 3. Both the peak amplitude and the duration of the after-hyperpolarization following an action potential were reversibly increased with increasing concentration of ouabain. In tetraethylammonium (TEA, 10-20 mM) and tetrodotoxin (TTX, 1-10 microM), the duration of both the calcium-dependent action potential and the after-hyperpolarization following the action potential was prolonged by ouabain (greater than or equal to 10 nM). 4. A depolarizing command pulse evoked a slow outward current in TEA (10-20 mM) and TTX (1-10 microM). This was increased in amplitude and prolonged in duration by ouabain (100 nM-1 microM). Such augmentation of the slow outward current by ouabain was usually associated with an increase in a slow inward current during the period of the depolarizing command pulse. 5. An outward current produced by the calcium ionophore A23187 was reversibly augmented by ouabain (greater than or equal to 10 nM). 6. An outward current caused by exchanging a potassium-free superfusion solution for one containing 4.7 or 10 mM-potassium was completely abolished by ouabain (greater than or equal to 10 nM). 7. The hyperpolarization elicited by intracellular injection of calcium was reversibly prolonged by either ouabain (1 microM) or caffeine (10 nM). 8. These results suggest that ouabain augments the after-hyperpolarization both by an increase in calcium influx across the cellular membrane and by an increase in intracellular calcium concentration.




This article has been cited by other articles:


Home page
J. Neurophysiol.Home page
K. A. Moore, A. S. Cohen, J. P. Y. Kao, and D. Weinreich
Ca2+-Induced Ca2+ Release Mediates a Slow Post-Spike Hyperpolarization in Rabbit Vagal Afferent Neurons
J Neurophysiol, February 1, 1998; 79(2): 688 - 694.
[Abstract] [Full Text] [PDF]


Home page
J. Pharmacol. Exp. Ther.Home page
J.-Q. Kong, J. A. Leedham, D. A. Taylor, and W. W. Fleming
Evidence that Tolerance and Dependence of Guinea Pig Myenteric Neurons to Opioids Is a Function of Altered Electrogenic Sodium-Potassium Pumping
J. Pharmacol. Exp. Ther., February 1, 1997; 280(2): 593 - 599.
[Abstract] [Full Text]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1987 The Physiological Society.