Although it is well known that neural control of gastric motility occurs via sympathetic, parasympathetic, noncholinergic, and nonadrenergic fibers contained in the vagus nerve, the central sites of origin of these influences are largely unknown. Recent experiments in our laboratory indicate that noncholinergic neural pathways originating in the posterior hypothalamus can markedly influence gastric motility. At least 2 weeks prior to the experiment, mongrel dogs were surgically prepared with bipolar recording electrodes fixed to the serosal surface of the stomach. This prevented violation of the abdominal cavity on the day of testing. Experiments were performed with the animals under alpha-chloralose anesthesia (100 mg kg-1) in temperature-controlled settings. Under stereotactic guidance, bipolar stimulation of the posterior periventricular hypothalamus produced profound reproducible excitatory or inhibitory effects on gastric myoelectric and motor activity. Changes in the frequency and amplitude of pacesetter potentials (PPs) and in the incidence of action potentials associated with them were observed. Stimulation of various loci in 14 dogs resulted in a 71 +/- 7.5% increase in the incidence of action potentials associated with gastric PPs in "excitatory" areas (n = 7) and a 69.1 +/- 4% decrease in this ratio in "inhibitory" areas (n = 19). In general, more lateral stimulation produced greater inhibitory effects. Responses were frequency dependent, with a threshold greater than 25 Hz in most cases. Excitatory gastric responses to hypothalamic stimulation occurred despite full systemic atropinization (0.1 mg kg-1). The physiologic significance of these noncholinergic excitatory pathways influencing distal gastric motility and the neurotransmitters they employ are as yet unknown.