Retrotrapezoid nucleus and central chemoreception

The ‘distributed chemoreception theory’ attributes the central chemoreflex (the stimulation of breathing by CNS acidification) to the cumulative effects of pH on multiple classes of respiratory neurons as well as on their tonic sources of drive. Opinions differ as to how many classes of pH-sensi...

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Bibliographic Details
Published inThe Journal of physiology Vol. 586; no. 8; pp. 2043 - 2048
Main Authors Guyenet, Patrice G., Stornetta, Ruth L., Bayliss, Douglas A.
Format Journal Article
LanguageEnglish
Published Oxford, UK The Physiological Society 15.04.2008
Blackwell Publishing Ltd
Blackwell Science Inc
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Summary:The ‘distributed chemoreception theory’ attributes the central chemoreflex (the stimulation of breathing by CNS acidification) to the cumulative effects of pH on multiple classes of respiratory neurons as well as on their tonic sources of drive. Opinions differ as to how many classes of pH-sensitive neurons contribute to the central chemoreflex but the number of candidates is high and growing fast. The ‘specialized chemoreceptor theory’, endorsed here, attributes the chemoreflex to a limited number of specialized neurons. These neurons (the central chemoreceptors) would drive a respiratory pattern generator that is not or minimally activated by acidification. In this review we first describe the properties of the retrotrapezoid nucleus (RTN) and argue that this nucleus may contain the most important central chemoreceptors. Next, we subject the assumptions that underlie the distributed chemoreception theory to a critical analysis. We propose several explanations for the apparent contradiction between the two competing theories of central chemoreception. We attribute much of the current controversy to premature extrapolations of the effects of acidification on neurons recorded in vitro (chemosensitivity) and to a semantic confusion between chemosensitivity and chemoreception (the mechanism by which CO 2 or pH activates breathing in vivo ).
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ISSN:0022-3751
1469-7793
1469-7793
DOI:10.1113/jphysiol.2008.150870