Journal of Neurophysiology, Vol 55, Issue 6 1234-1246, Copyright © 1986 by APS
Afterhyperpolarization mechanisms in cat sympathetic preganglionic neuron in vitro
M. Yoshimura, C. Polosa and S. Nishi
A long-lasting afterhyperpolarization (AHP) follows the antidromic or
current-induced action potential of sympathetic preganglionic neurons
(SPNs) studied in slices of cat spinal cord maintained in vitro. Duration
and amplitude of the AHP that follows a single spike were 2.8 +/- 0.3 s and
16.0 +/- 0.7 mV (mean +/- SE), respectively. In most cases two components
could be distinguished, an initial faster and usually larger component
[fast (F) AHP] followed by a slowly decaying component [slow (S) AHP]. An
increase in membrane conductance was associated with the AHP. The amplitude
of both components increased with membrane depolarization and decreased
with hyperpolarization. Both fast and slow component were nullified at a
voltage of -90 mV in 3.6 mM K+. Peak AHP amplitude decreased as K+ was
increased from 1.5 to 7.0 mM. The null point for both fast (F) AHP and slow
(S) AHP shifted in the depolarizing or hyperpolarizing direction when K+
was increased or decreased, respectively. These data suggest that an
increase in K+-conductance is the mechanism underlying the AHP. The two
components of the AHP could be separated by their differential sensitivity
to superfusion with the Ca2+-channel blocker cobalt (2 mM) or with low Ca2+
(0.25 mM). These procedures resulted in an AHP of much shorter duration
(330 ms, range 150-600), presumably the FAHP. These observations indicate
that a Ca2+-activated K+-conductance is likely to be involved in the
generation of the SAHP. The FAHP was depressed during superfusion with
tetraethylammonium (TEA) (20 mM) and intracellular cesium injection. The
SAHP was enhanced by TEA and enhanced or depressed by cesium. In 3.6 mM K+
the FAHP reversed in polarity at membrane voltages more negative than -90
mV. This component had an approximately linear relation of amplitude to
membrane potential. The SAHP did not reverse in most cells. In the few
cases in which it reversed, the change in amplitude for a given change in
membrane voltage was much smaller on the negative than on the positive side
of the null potential. Thus the SAHP shows voltage-dependent, nonlinear
characteristics. This difference in behavior of the two components was also
observed when the null point was displaced in high or low K+. In the
presence of tetrodotoxin (TTX) the AHP persisted in temporal association
with a high-threshold, TTX-resistant, cobalt-sensitive spike. During the
time course of the AHP the efficacy of synaptic input decreased, suggesting
that the AHP has an important role in regulating the firing rate of the
SPN.
