Association between vagal afferent nerve fibers and mast cells in rat jejunal mucosa

1995 ◽  
Vol 108 (4) ◽  
pp. A941 ◽  
2008 ◽  
Vol 104 (5) ◽  
pp. 1394-1401 ◽  
Author(s):  
David F. Donnelly

The mechanism by which action potentials (APs) are generated in afferent nerve fibers in the carotid body is unknown, but it is generally speculated to be release of an excitatory transmitter and synaptic depolarizing events. However, previous results suggested that Na+ channels in the afferent nerve fibers play an important role in this process. To better understand the potential mechanism by which Na+ channels may generate APs, a mathematical model of chemoreceptor nerve fibers that incorporated Hodgkin-Huxley-type Na+ channels with kinetics of activation and inactivation, as determined previously from recordings of petrosal chemoreceptor neurons, was constructed. While the density of Na+ channels was kept constant, spontaneous APs arose in nerve terminals as the axonal diameter was reduced to that in rat carotid body. AP excitability and pattern were similar to those observed in chemoreceptor recordings: 1) a random pattern at low- and high-frequency discharge rates, 2) a high sensitivity to reductions in extracellular Na+ concentration, and 3) a variation in excitability that increased with AP generation rate. Taken together, the results suggest that an endogenous process in chemoreceptor nerve terminals may underlie AP generation, a process independent of synaptic depolarizing events.


1981 ◽  
Vol 240 (2) ◽  
pp. H190-H198 ◽  
Author(s):  
J. E. Angell-James ◽  
R. Elsner ◽  
M. De Burgh Daly

In the anesthetized harbor seal, Phoca vitulina, the Hering-Breuer inflation reflex was weak and comparable to that in humans. Single inflations of the lungs from a syringe during the expiratory phase of normal breathing caused temporary inhibition of breathing and an immediate tachycardia dependent on the integrity of the cervical vagosympathetic nerves. A similar cardiac response occurred when the lungs were artificially inflated during an experimental dive and under conditions in which apnea and bradycardia were reflexly induced by a combination of stimulation of the carotid body chemoreceptors and of the trigeminal or laryngeal input. Recordings from single vagal afferent nerve fibers innervating presumptive pulmonary stretch receptors showed a close relationship between the increase in impulse frequency and increase in lung volume or transpulmonary pressure. It appears that in diving the decrease in pulmonary stretch receptor activity during apnea, combined with cessation of central inspiratory neuronal drive, is an important integrative mechanism that helps development of the reflex bradycardia of trigeminal, carotid, chemoreceptor, and baroreceptor origin.


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