A. Sawczuk et al., CONTRIBUTION OF OUTWARD CURRENTS TO SPIKE-FREQUENCY ADAPTATION IN HYPOGLOSSAL MOTONEURONS OF THE RAT, Journal of neurophysiology, 78(5), 1997, pp. 2246-2253
Spike-frequency adaptation has been attributed to the actions of sever
al different membrane currents. In this study, we assess the contribut
ions of two of these currents: the net outward current generated by th
e electrogenic Na+-K+ pump and the outward current that flows through
Ca2+-activated K+ channels. In recordings made from hypoglossal motone
urons in slices of rat brain stem, we found that bath application of a
4-20 mu M ouabain solution produced a partial block of Na+-K+ pump ac
tivity as evidenced by a marked reduction in the postdischarge hyperpo
larization that follows a period of sustained discharge. However, we o
bserved no significant change in either the initial, early, or late ph
ases of spike-frequency adaptation in the presence of ouabain. Adaptat
ion also has been related to increases in the duration and magnitude o
f the medium-duration afterhyperpolarization (mAHP) mediated by Ca2+-a
ctivated K+ channels. When we replaced the 2 mM Ca2+ in the bathing so
lution with Mn2+, there was a significant decrease in the amplitude of
the mAHP after a spike. The decrease in mAHP amplitude resulted in a
decrease in the magnitude of the initial phase of spike-frequency adap
tation as has been reported previously by others. However, quite unexp
ectedly we also found that reducing the mAHP resulted in a dramatic in
crease in the magnitude of both the early and late phases of adaptatio
n. These changes could be reversed by restoring the normal Ca2+ concen
tration 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 su
pport the hypothesis that initial adaptation is, in part, controlled b
y conductances underlying the mAHP. However, our failure to eliminate
initial adaptation completely by blocking Ca2+ channels suggests that
other membrane mechanisms also contribute. Finally, the increase in bo
th the early and late phases of adaptation in the presence of Mn2+ blo
ck of Ca2+ channels lends further support to the hypothesis that the i
nitial and later (i.e., early and late) phases of spike-frequency adap
tation are mediated by different cellular mechanisms.