CONTRIBUTION OF OUTWARD CURRENTS TO SPIKE-FREQUENCY ADAPTATION IN
HYPOGLOSSAL MOTONEURONS OF THE RAT.
Andrea Sawczuk, Randall K. Powers and Marc D. Binder.
Department of Physiology & Biophysics, University of Washington, School of
Medicine, Seattle, Washington 98195 USA.
APStracts 4:143N, 1997.
ABSTRACT
Spike-frequency adaptation has been attributed to the actions of several
different membrane currents. In this study, we assess the contributions of two
of these currents: The net outward current generated by the electrogenic Na+-
K+ pump and the outward current that flows through Ca2+-activated K+ channels.
In recordings made from hypoglossal motoneurons in slices of rat brain stem,
we found that bath application of a 4-20 æM ouabain solution produced a
partial block of Na+-K+ pump activity as evidenced by a marked reduction in
the post-discharge hyperpolarization (PDH) that follows a period of sustained
discharge. However, we observed no significant change in either the initial,
early or late phases of spike-frequency adaptation in the presence of ouabain.
Adaptation has also been related to increases in the duration and magnitude of
the medium-duration afterhyperpolarization (mAHP) mediated by Ca2+-activated
K+ channels. When we replaced the 2 mM Ca2+ in the bathing solution with Mn2+,
there was a significant decrease in the amplitude of the mAHP following a
spike. The decrease in mAHP amplitude resulted in a decrease in the magnitude
of the initial phase of spike-frequency adaptation, as has been previously
reported by others. However, quite unexpectedly we also found that reducing
the mAHP resulted in a dramatic increase in the magnitude of both the early
and late phases of adaptation. These changes could be reversed by restoring
the normal Ca2+ concentration in the bath. Our results with ouabain indicate
that the Na+-K+ pump plays little, if any, role in the three phases of
adaptation in rat hypoglossal motoneurons. Our results with Ca2+ channel
blockade support the hypothesis that initial adaptation is, in part,
controlled by conductances underlying the mAHP. However, our failure to
completely eliminate initial adaptation by blocking Ca2+ channels suggests
that other membrane mechanisms also contribute. Finally, the increase in both
the early and late phases of adaptation in the presence of Mn2+ - block of
Ca2+ channels lends further support to the hypothesis that the initial and
later (i.e., early and late) phases of spike-frequency adaptation are mediated
by different cellular mechanisms.
Received 10 February 1997; accepted in final form 2 July 1997.
APS Manuscript Number J120-7.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 27 August 1997