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Abstract
Previous studies of vagal control of GI function report that vagal efferent nerves originating in the dorsal motor nucleus of the vagus (DMV) provide functional control over gastric motility. These vagal efferent nerves are reported to consist of parallel excitatory and inhibitory pathways. In contrast, recent studies in the rat were unable to demonstrate an inhibitory pathway originating in the DMV. The purpose of my research was to functionally characterize the DMV vagal pathways that are responsible for controlling gastric motility. I used several different approaches in my study: (1) assessment of vagotomy on L-glutamate-induced gastric responses evoked from the DMV and mNTS; (2) attempts to unmask an inhibitory DMV pathway using systemically administered L-NAME, atropine methyl bromide and bethanechol; (3) replication of key experiments that provided evidence of an inhibitory DMV vagal pathway; (4) assessment of the effect of baclofen, an agent thought to activate the inhibitory DMV pathway; and (5) assessment of NTS-induced inhibition of gastric motility. In the first approach, I unilaterally microinjected L-glutamate (500pmol/34nl) into the intermediate DMV and mNTS of anesthetized rats while monitoring intragastric pressure (IGP) and blood pressure. Microinjection into the DMV increased the IGP (4.5 ± 0.7 mmHg, n=8). This effect was abolished by ipsilateral vagotomy and atropine. The excitatory effect of L-glutamate on IGP was never augmented by L-NAME. Microinjection of L-glutamate into the mNTS reduced IGP by -1.0 ± 0.2 mmHg (n=6). This decrease was unaffected by ipsilateral vagotomy, but was abolished by bilateral vagotomy. Microinjection of agents previously shown to produce gastric relaxation from the DMV (e.g., substance P, NMDA, and oxytocin) only evoked increases in gastric motility that were blocked by ipsilateral vagotomy. Blockade of decreases in motility required bilateral vagotomy, indicating diffusion of drug to the mNTS. CRF failed to have any gastric effects upon microinjection into the DMV. Baclofen microinjected into the DMV produced gastric excitation, which was prevented by both atropine and ipsilateral vagotomy. NTS-induced inhibition of gastric motility was unaffected L-NAME. These data indicate that the physiologically important pathway from the DMV to the stomach is a cholinergic-cholinergic excitatory pathway.
