The effects of halothane on ganglionic transmission were studied by recording extracellular potentials from the postganglionic nerve of the isolated hamster stellate ganglion. Halothane, at concentrations greater than 0.1 mM, decreased the potentials evoked by preganglionic stimuli at 0.2 Hz. Halothane also blocked discharges elicited by 1,1-dimethyl-4-phenylpiperazinium, a selective nicotinic agonist, and discharges elicited by the nicotinic actions of exogenous acetylcholine. Repetitive preganglionic stimulation (30 Hz, 5 seconds) in the presence of nicotine (10(-3) M), or hexamethonium (10(-3) M), evoked asynchronous discharges in the postganglionic nerve. These discharges were suppressed by low concentrations of atropine, and were probably due to the muscarinic actions of neurotransmitter. Halothane depressed these discharges at approximately the same concentration that it depressed the compound action potential elicited by low frequency preganglionic stimulation in the untreated ganglion. Halothane had no effect on the discharges elicited by 4-(m-chlorophenylcarbamoyloxy)-2-butynyltrimethylammonium chloride (McN-A-343), a selective muscarinic agonist, or the discharges elicited by the muscarinic actions of acetylcholine. These results are most readily explained by hypothesizing that halothane acts at two sites in the ganglion. It appears to depress the postsynaptic response to the nicotinic actions of the neurotransmitter, acetylcholine. Also, it probably depresses transmitter release from the presynaptic nerve endings during repetitive stimulation.
(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium Chloride Acetylcholine