Skip to main content

Sensory Signal Transduction in the Vagal Primary Afferent Neurons

Buy Article:

$55.00 plus tax (Refund Policy)

The vagal nerve conveys primary afferent information from the intestinal mucosa to the brain stem. Activation of vagal afferent fibers results in inhibition of food intake, gastric emptying, and stimulation of pancreatic secretion. Afferents nerves terminating near to the mucosa are in a position to monitor the composition of the luminal contents. As afferents do not project directly into the lumen, their activation depends on an intermediary step, i.e. neuronal activation by a secondary substance released from within the mucosal epithelium. This review addresses the role for both cholecytokinin (CCK) and serotonin (5-HT) released from enteroendocrine cells and acting as paracrine agents on the terminals of vagal afferents in responses to a number of luminal signals. CCK acted on both high- and lowaffinity CCK-A receptors present on distinct vagal primary afferent neurons. Neurons of the nodose ganglia respond to intraduodenal perfusions of maltose, glucose, and hypertonic saline. These neurons were also sensitive to exogenous luminally applied 5-HT at concentrations that mimic physiologic levels. Intravenous administration of a 5-HT3 antagonist blocked these responses suggesting that nodose neuronal responses to luminal osmolarity and to the digestion products of carbohydrates are dependent on the release of endogenous 5- HT from the mucosal enterochromaffin (EC) cells, which acts on the 5-HT3 receptors on vagal afferent fibers to stimulate vagal afferent neurons. Double-labeling studies revealed that nodose neurons responded to 5-HT-dependent luminal stimuli contain mainly glutamate and substance P. Over the past year or so it has become clear that there are multiple possible excitatory inputs to a common vagal afferent route with synergistic interactions being common. The nodose ganglion contains neurons that may possess only high- or low-affinity CCK-A receptors or 5-HT3 receptors. Some neurons that express high-affinity CCK-A receptors also express 5-HT3 receptors and (or) secretin receptors. Pre-exposure to luminal 5-HT may augment the subsequent response to a subthreshold dose of CCK. Synergistic interaction between CCK and secretin also occurs at the nodose ganglia; this is mediated by high affinity CCK-A receptor. This may explain the robust postprandial secretion of enzyme, bicarbonate, and fluid despite the modest increase in CCK after a meal. Some neurons that possess low-affinity CCK-A receptor colocalize with leptin receptors (OB-Rs). These neurons also respond to mechanical distention. Interaction between CCK-A receptor and OB-Rs in these neurons likely facilitates leptin mediation of short-term satiety.
No References
No Citations
No Supplementary Data
No Article Media
No Metrics

Keywords: Cholecytokinin; Endocrine and Enterochromaffin cells; Macronutrients; Nodose ganglia; Sensory transduction; Serotonin; Synergistic interactions; Vagus nerve

Document Type: Research Article

Affiliations: Department of Internal Medicine, Division of Gastroenterology, University of Michigan, 6510 Medical Sciences Research Building I, 1150 West Medical Center Drive, Ann Arbor, MI 48109-0682, USA.

Publication date: 2007-10-01

More about this publication?
  • Current Medicinal Chemistry covers all the latest and outstanding developments in medicinal chemistry and rational drug design. Each issue contains a series of timely in-depth reviews written by leaders in the field covering a range of the current topics in medicinal chemistry. Current Medicinal Chemistry is an essential journal for every medicinal chemist who wishes to be kept informed and up-to-date with the latest and most important developments.
  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content
Cookie Policy
X
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more