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Interactions of chemostimuli at the single cell level: studies in a model system
Author(s) -
Peers Chris
Publication year - 2004
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2003.002657
Subject(s) - carotid body , chemoreceptor , neuroscience , depolarization , stimulus (psychology) , exocytosis , membrane potential , biophysics , hypercapnia , chemistry , electrophysiology , afferent , biology , hypoxia (environmental) , anatomy , respiratory system , membrane , receptor , psychology , oxygen , biochemistry , organic chemistry , psychotherapist
The responses of afferent chemosensory fibres of the carotid body to individual chemostimuli have long been established. However, the mechanisms underlying the multiplicative interactions of these stimuli (i.e. how the combined effects of hypoxia and hypercapnia exert a greater effect on afferent nerve discharge than the sum of their individual effects) have not been elucidated. Using the membrane hypothesis for carotid body chemoreception, in which chemostimuli inhibit type I cell K + channels, leading to depolarization, voltage‐gated Ca 2+ entry and hence the triggering of exocytosis, this article considers data acquired in isolated type I carotid body cells and model chemoreceptor (PC12) cells to attempt to explain stimulus interactions. Whilst stimulus interactions are not clearly evident at the level of K + channel inhibition or rises of [Ca 2+ ] i , they are apparent at the level of transmitter release. Thus, it is clear that individual chemoreceptor cells can sense multiple stimuli, and that interactions of these stimuli can produce greater than additive effects in terms of transmitter release.