Acetylcholine causes nicotinic depolarization in rat dorsal motor nucleus of the vagus, in vitro.

Action of acetylcholine (ACh) on the electrophysiologically identified preganglionic neurons in the dorsal motor nucleus of the vagus (DMV) were investigated in slice preparations of rat medulla oblongata by using conventional intracellular recording technique. Applications of ACh to the DMV neurons resulted in a marked depolarization, which was not abolished in Ca-free superfusing solution, indicating the direct action of ACh on the cells. This depolarization was associated with an increase in membrane conductance and markedly reduced in the Na-free superfusate. The extrapolated reversal potential of ACh response was about -35 mV, indicating that both sodium and potassium conductances are likely responsible for the ACh depolarization. Application of nicotine caused similar depolarization to that of ACh, while muscarinic agonists (muscarine and oxotremorine) did not have any effect. Additions of the nicotinic antagonists hexamethonium and D-tubocurarine to the bathing solution reversibly attenuated the ACh-induced depolarization, while the muscarinic antagonist atropine did not have any effect. The nicotinic properties of ACh action in the DMV neurons presented here form a striking contrast to previous autoradiographic findings. Though endogenous cholinergic inputs to the DMV have not been identified, ACh may have a strong influence on vagal control by depolarization through nicotinic receptors of the DMV preganglionic neurons.