The location of the chemoreceptor controlling growth hormone secretion during hypoglycemia in primates.
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We report that the afferent relays of visceral (cardiovascular, digestive and respiratory) reflexes, differentiate under the control of the paired-like homeobox gene Phox2b: the neural crest-derived carotid body, a chemosensor organ, degenerates in homozygous mutants, as do the three epibranchial placode-derived visceral sensory ganglia (geniculate, petrosal and nodose), while their central target, the nucleus of the solitary tract, which integrates all visceral information, never forms. These data establish Phox2b as an unusual 'circuit-specific' transcription factor devoted to the formation of autonomic reflex pathways. We also show that Phox2b heterozygous mutants have an altered response to hypoxia and hypercapnia at birth and a decreased tyrosine hydroxylase expression in the petrosal chemosensory neurons, thus providing mechanistic insight into congenital central hypoventilation syndrome, which is associated with heterozygous mutations in PHOX2B.
Vertebrate olfactory and gustatory receptors are necessarily exposed to the fluid which contains their relevant chemosensory environment. In terrestrial mammals, the nasal airways serve as protective accessory tissues for the olfactory receptors, but tastes receptors in all vertebrates and olfactory receptors in fish are directly exposed to the liquids which bring chemosensory stimuli to them. The differentiated epithelial cells which form taste buds and the specialized neurons which are the vertebrate olfactory receptors are constantly replaced in normal adult animals, suggesting that chemosensory function per se is damaging to the receptors. Organic and sulfur-containing air pollutants may be among those which adversely affect olfactory receptors, but adequate data are not available. Surfactants and heavy metals can produce physiological and/or morphological damage in gustatory receptors. Some heavy metals are concentrated in saliva, a liquid which interacts closely with taste receptors. A failure to evaluate human chemosensory function in relation to potential chemosensory toxicants accounts for the present inability to specify the incidence of the problem.
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Previous study has revealed that water-responsive afferent neurons in the superior laryngeal nerve induced inhibition of motility in the proximal and distal stomach using anaesthetized rats. These gastric responses might facilitate the reservoir function of the stomach. To confirm the gastric responses discovered in rats also occur in humans, we evaluated gastric myoelectrical activities in healthy volunteer subjects during fluid intake using electrogastrography. Before human experiments, we recorded the myoelectrical activities in rats to evaluate the response induced by the administration of water into the larynx. A large deflection in the gastric myoelectrical activities was observed just after the administration of water in anesthetized rats. A similar large deflection was also observed just after voluntary swallowing of 20 ml water in humans. The swallowing of saliva did not induce such response. We further observed the gastric response during reflex swallowing elicited by slow infusion of isotonic saline, water or 0.05 M citric acid on to the posterior tongue. Infusion of water and citric acid but not 0.15 M saline induced significant changes in mean relative ratio of the response. These electrogastrographic responses induced by the infusion of liquids strongly suggest that the gastric motor response facilitates reservoir function of the stomach during liquid intake in humans as well as in rats.
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