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The Johns Hopkins Asthma and Allergy Center, Baltimore, Maryland 21224-6821
Intracellular microelectrode recordings were
obtained from neurons located in adult guinea pig bronchial
parasympathetic ganglia in situ to determine the calcium and potassium
currents regulating repetitive action potential activity and firing
rates by these neurons. Neurons in these ganglia respond to prolonged
suprathreshold depolarizing current steps with either a burst of action
potentials at the onset of the stimulus (accommodating or phasic
neurons) or repetitive action potentials throughout the stimulus
(nonaccommodating or tonic neurons). Instantaneous and adapted firing
rates during prolonged threshold and suprathreshold stimuli were lower
in tonic than in phasic neurons, indicating a longer interspike
interval between repetitive action potentials in tonic neurons. In
tonic neurons, blockade of A-type current with 4-aminopyridine
increased accommodation; 4-aminopyridine or apamin decreased the
interspike interval in tonic neurons. Calcium-free buffer, cadmium
ions, or 
-conotoxin GVIA also increased accommodation in tonic
neurons but did not affect the interspike interval; nifedipine or
verapamil did not affect the tonic firing pattern. Accommodation in
phasic neurons could be decreased by a conditioning hyperpolarization step of the resting potential, which could be subsequently blocked by
4-aminopyridine or calcium-free buffer. Accommodation in phasic neurons
could also be decreased by apamin or barium ions: the repetitive action
potentials observed during these treatments could be reversed by
cadmium ions or calcium-free buffer. These results indicate that tonic
and phasic neurons in guinea pig bronchial parasympathetic ganglia have
similar types of calcium currents, but potassium channels may
ultimately regulate the accommodation pattern, the firing rate, and,
consequently, the output from these neurons.
parasympathetic; tonic neurons; phasic neurons; trachea; bronchoconstriction; calcium channels; potassium channels; N-type
channel; -conotoxin GVIA; apamin; 4-aminopyridine
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