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The Journal of Neurophysiology Vol. 81 No. 5 May 1999, pp. 2164-2174
Copyright ©1999 by the American Physiological Society
1 Agonist Methoxamine
Department of Physiology and Department of Physical Medicine and Rehabilitation, Northwestern University Medical School, Chicago, Illinois 60611
Lee, R. H. and
C. J. Heckman.
Enhancement of Bistability in Spinal Motoneurons In Vivo by the
Noradrenergic 1 Agonist Methoxamine. J. Neurophysiol. 81: 2164-2174, 1999.
Enhancement of bistability in spinal motoneurons in vivo by the
noradrenergic 
1 agonist methoxamine. Like many
types of motoneurons, spinal motoneurons in the adult mammal can
exhibit bistable behavior. This means that short periods of excitatory
input can initiate long periods of self-sustained firing and that
equally short periods of inhibition can return the cell to the
quiescent state. Usually, the presence of one of the monoamines (either
serotonin or norepinephrine) is required for spinal motoneurons to
express bistable behaviors. Because the decerebrate cat preparation has
tonic activity in monoaminergic fibers that originate in the brain stem
and project to spinal motoneurons, these cells sometimes exhibit
bistable behavior. However, exogenous application of the noradrenergic 1 agonist methoxamine greatly enhances bistable behavior
in the decerebrate. The goal of this study was to identify the
mechanisms of this action of methoxamine. The total persistent inward
current (IPIC) in spinal motoneurons in the
decerebrate cat was measured from I-V functions generated by
triangular voltage commands applied using discontinuous single
electrode voltage clamp. The effect of methoxamine on
IPIC was assessed by comparing its properties in
a control cell sample without methoxamine to its properties in a sample
of cells obtained after application of methoxamine. In most
experiments, at least one cell was obtained from each sample. Our
results showed that methoxamine approximately doubled the amplitude of
IPIC without changing its onset voltage, its offset voltage, or its persistence. The reduced amplitude was a
consistent finding within experiments and so was unlikely to be caused
by interanimal variability. In addition, methoxamine depolarized
motoneurons without altering their input conductances, so that a
smaller amount of current was required to reach the onset voltage of
IPIC. These effects of methoxamine were
approximately equal in all cells. As a result of these changes,
methoxamine greatly enhanced the tendency for motoneurons to become
bistable. It is proposed that the methoxamine-induced increase in the
amplitude of IPIC is effective in enhancing the
duration of bistable firing because this increase makes
IPIC more resistant to the deactivating effects
of the afterhyperpolarizations between spikes.
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