Ac. Myers et Bj. Undem, ANTIGEN DEPOLARIZES GUINEA-PIG BRONCHIAL PARASYMPATHETIC GANGLION NEURONS BY ACTIVATION OF HISTAMINE H-1 RECEPTORS, American journal of physiology. Lung cellular and molecular physiology, 12(6), 1995, pp. 879-884
Studies were carried out to evaluate the mechanism by which neurotrans
mission through airway parasympathetic ganglia may be modulated during
immediate hypersensitivity reactions. Guinea pigs were passively sens
itized by injection of guinea pig serum containing high-titer anti-ova
lbumin antibodies. Intracellular recordings were obtained from intrins
ic parasympathetic ganglion neurons from the right mainstem bronchus i
n vitro. Ovalbumin (10 mu g/ml) elicited a membrane potential depolari
zation and changes in membrane resistance in bronchial ganglion neuron
s from passively sensitized guinea pigs. Histamine mimicked the depola
rizing effect of ovalbumin in a concentration-dependent manner (0.1-10
mu M) and caused a transient increase and decrease in membrane resist
ance. Pyrilamine, a histamine H-1-receptor antagonist, inhibited the h
istamine-induced membrane depolarization and decrease in resistance. B
y contrast, blocking histamine H-2 and H-3 receptors did not inhibit h
istamine-induced depolarization. Pyrilamine also reduced the antigen-i
nduced depolarization of ganglion neurons, demonstrating a role for hi
stamine H-1 receptors in this response. The data provide evidence that
the antigen-induced depolarization of airway ganglion neurons is seco
ndary to an antigen-antibody interaction on intrinsic mast cells and t
he consequential effect of histamine on H-1 receptors. These studies d
emonstrate that histamine released during an immediate hypersensitivit
y reaction has direct effects on airway parasympathetic nerves.