An electrogenic pump and a Ca2+-dependent K+ conductance contribute to a posttetanic hyperpolarization in lamprey sensory neurons. Parker, David, Russell Hill and Sten Grillner. Nobel Institute of Neurophysiology, Department of Neuroscience, Karolinska Institute, S-17177, Stockholm, Sweden.
APStracts 3:0040N, 1996.
(1) Tetanic stimulation of lamprey sensory dorsal cells resulted in a posttetanic hyperpolarization (PTH). The amplitude and duration of the PTH was dependent on the stimulus duration and frequency. The PTH was not reversed at membrane potentials negative to -100mV, whereas the afterhyperpolarization following single action potentials reversed at approximately -85mV. There was also a biphasic effect on the input resistance during the PTH, with an early reduction that recovered to control before the PTH had decayed. (2) The amplitude and duration of the PTH were increased in Ringer containing TEA and 4-AP, both of which broadened single action potentials, but reduced following intracellular injection of Cs+. Ca2+-free Ringer, Cd2+ and Co2+ also reduced the PTH, suggesting the involvement of a Ca2+-dependent K+ conductance. However, the PTH was not reduced in Ba2+ Ringer, or by the Ca2+-dependent K+ channel antagonists apamin and charybdotoxin. (3) The cardiac glycoside ouabain reduced the amplitude and duration of the PTH, as did substitution of Na+ with choline or Li+. K+-free Ringer also reduced the PTH, whereas high K+ Ringer had more variable effects. The amplitude and duration of the PTH were also dependent on temperature. These results support the involvement of an ouabain-sensitive Na-K pump in the PTH. (4) The PTH was reduced by the tachykinins substance P and physalaemin, and by 5-HT, which blocks apamin- sensitive Ca2+-dependent K+ channels in the lamprey. However, GABA, which has been reported to reduce a Ca2+-dependent K+ conductance in the dorsal cells, did not reduce the PTH. (5) These results suggest that a Ca2+-dependent K+ conductance and a Na-K electrogenic pump underlie the PTH. The PTH reduces the excitability of the dorsal cells, suggesting that it may act as a mechanism to gate sensory information entering the spinal cord.

Received 7 November 1995; accepted in final form 5 February 1996.
APS Manuscript Number J753-5.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 14 February 96