Functional effects and characteristics of cecum-projecting neurons in the dorsal motor nucleus of the vagus of rats.

Preganglionic neurons in the dorsal motor nucleus of the vagus (DMV) innervate most of the gastrointestinal tract; with the stomach and the cecum/proximal colon having a greater proportion of vagal input. Cecum-projecting neurons have been thought to be distinct from other preganglionic neurons due to their location within the DMV, but it is unknown whether these neurons innervate the cecum exclusively or what effect their activation has on cecal motor activity. Therefore, we investigated the extent of coinnervation of cecum and stomach by vagal neurons, their neurochemistry, and the effect of DMV stimulation on intracecal and intragastric volumes. Fluorescent retrograde tracers injected into the serosa of the cecum and stomach revealed that in the DMV 49+/-5% CTB-labeled cecum-projecting neurons also innervated the stomach. Immunocytochemical staining for nitric oxide (NO) synthase and tyrosine hydroxylase indicated that only 3+/-1% and 4+/-1% of cecum-projecting neurons contained these markers, respectively. In anesthetized rats gastric and cecal volumes were measured by prototypic miniaturized dual barostats that were developed for use in rodents. Microinjection of l-glutamate into the DMV increased gastric contractile activity and tone, and reduced on-going cecum contractile activity (2.6+/-0.7 contractions/2 min after injection versus 8.2+/-0.4 contractions/2 min before injection, N = 5). The barostat was able to detect decreases (-0.88+/-0.13 ml) and increases (0.25+/-0.05 ml) in cecum volume in response to carbachol and sodium nitroprusside, respectively. In summary, cecum-projecting neurons are not an entirely exclusive population within the DMV because a percentage of these also innervate the stomach. Central vagal stimulation can modulate both gastric and cecum contractile activity. Together, these data support a role of the vagus in neural reflexes involving gastric and large bowel motor function, such as the immediate phase of the gastrocolonic reflex.

Central mechanisms of lower esophageal sphincter control.

Lower esophageal sphincter (LES) tone is decreased during swallowing, during transient LES relaxations (TLESRs), and before emesis, and this decrease is due primarily to increasing inhibitory vagal output to the LES. Reflex-evoked relaxation of the LES is mediated by long-loop vagovagal reflexes that are coordinated by the dorsal vagal complex in the hindbrain medulla. A sequence of events occurs. Central control of TLESRs has not been studied directly; the information on how drugs may work centrally to reduce TLESRs is extrapolated from knowledge of how the brain evokes LES relaxation. Reduction of the frequency of TLESRs by a GABAB agonist, baclofen, is due to inhibition of vagal afferents, information transfer between the nucleus tractus solitarius and dorsal motor nucleus of the vagus, and vagal efferent outflow. Preliminary data show that cannabinoid receptor activation reduces information transfer between the nucleus tractus solitarius and dorsal motor nucleus of the vagus. The potential therapeutic usefulness of these types of agents that reduce TLESRs by acting centrally is promising.