Properties of K+ currents were studied in isolated adult rat parasympa
thetic intracardiac neurones with the use of single-electrode voltage-
clamp techniques. A hyperpolarization-activated inward rectifier curre
nt was revealed when the membrane was clamped close to the resting lev
el (-60 mV). The slowly developing inward relaxation had a mean amplit
ude of 450 pA at -150 mV, an activation threshold of -60 to -70 mV and
a relaxation time constant of 41 ms at -120 mV. The current was rever
sibly blocked by Cs+ (1 mM) and became smaller with reduced [K+](0) an
d [Na+](0), indicating that this inward rectifier current probably is
a time- and voltage-dependent Na+-K+ current. 3. Step depolarizations
from the holding potential of -80 mV evoked a transient (< 100 ms at -
40 mV) outward K+ current (I-A) which was blocked by 4-aminopyridine (
4-AP, 1 mM). The time constants for I-A inactivation were 20 ms at -50
mV and 16 ms at -20 mV. The steady-state activation and (removal of)
inactivation curve showed a small overlap between -70 and -40 mV; the
reversal potential of I-A was close to E(K). 4. Step hyperpolarization
s from the depolarized potentials, i.e. -30 mV, revealed a slow inward
relaxation associated with the deactivation of a time- and voltage-de
pendent current. The inward relaxation became faster at more hyperpola
rized potentials and reversed at -85 and -53 mV in 4.7 and 15 mM [K+](
0). This current was blocked by muscarine (20 mu m) and Ba2+ (1 mM) bu
t not affected by Cs+(1 mM) this current may correspond to the M-curre
nt (I-M). 5. Depolarization-activated outward K+ currents were evoked
by holding the membrane close to the resting potential in the presence
of tetrodotoxin (TTX, 3 mu m), 4-AP (1 mM) and Ba2+ (1 mM). The ampli
tude of the outward relaxation and the tail current became smaller as
the [K+](0) was elevated. The outward tail current was reduced in a Ca
2+-free solution and the residual current was eliminated by the additi
on of tetraethylammonium (TEA, 10 mM); the reversal potential was shif
ted in a direction predicted by the Nernst eciuation. These findings s
uggest the presence of delayed rectifier K+ current and Ca2+-activated
K+ current. 6. Superfusion of TEA, Ba2+ and 4-AP, but not Cs+, induce
d rhythmic discharges in some of the otherwise quiescent intracardiac
neurones. 7. It is concluded that several K+ conductances are present
in adult rat intracardiac neurones and these currents working in conce
rt endow the neurones with a multitude of mechanisms to ensure proper
membrane excitability and firing pattern.