TRH/TRH-R1 receptor signaling in the brain medulla as a pathway of vagally mediated gut responses during the cephalic phase.
Level 5 - mechanism / opinion, no new human data
Narrative review of preclinical animal and mechanistic neurobiology studies
PubMed 23886382 · doi:10.2174/13816128113199990578
What was done
This narrative review summarizes preclinical laboratory research, primarily in rats and dogs, evaluating the role of medullary thyrotropin-releasing hormone (TRH) and its receptor TRH-R1 in the vagal control of gastric function during the cephalic phase of digestion.
What was found
The abstract provides no numerical data. It reports that TRH-synthesizing neurons project to TRH-R1-expressing neurons in the dorsal motor nucleus of the vagus (DMN). Injection of TRH into the DMN or cisterna magna increases vagal efferent activity and stimulates atropine-sensitive gastric acid, pepsin, serotonin, histamine, and ghrelin secretion, as well as gastric motility. Blocking central TRH signaling with antibodies or TRH-R1 antisense oligodeoxynucleotides abolishes sham-feeding-induced gastric acid secretion. The response is potentiated by serotonin and proTRH peptide Ps4, and suppressed by stress- or immune-related peptides.
Why it matters
It outlines the central medullary peptide circuitry that translates cephalic sensory inputs into vagally driven gastrointestinal motor and secretory activity.
Limits
The review relies entirely on preclinical animal experiments (rats and dogs) and mechanistic interventions; no human data, sample sizes, or quantitative statistical results are reported in the abstract.
Cited by
- supports The cephalic phase response increases salivation and gastric secretions to prepare the digestive system for incoming food.