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First published online January 8, 2007
Journal of Experimental Biology 210, 227-237 (2007)
Published by The Company of Biologists 2007
doi: 10.1242/jeb.02606

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Afferent input modulates the chronic hypercapnia-induced increase in respiratory-related central pH/CO₂ chemosensitivity in the cane toad (Bufo marinus)

Afshan Gheshmy, Ali Anari, Donela Besada and Stephen G. Reid^*

Centre for the Neurobiology of Stress, Department of Life Sciences, University of Toronto at Scarborough, 1265 Military Trail, Toronto, ON, M1C 1A4, Canada

^* Author for correspondence (e-mail: sgreid{at}utsc.utoronto.ca)

Accepted 17 October 2006

The goal of this study was to examine the role of respiratory-related afferent input on the chronic hypercapnia (CHC)-induced increase in central respiratory-related pH/CO₂ chemosensitivity in cane toads (Bufo marinus). Toads were exposed to CHC (3.5% CO₂) for 10 days, following which in vitro brainstem-spinal cord preparations were used to assess central respiratory-related pH/CO₂ chemosensitivity. Motor output from the vagus nerve root was used as an index of breathing (fictive breathing). Olfactory denervation (OD), prior to exposure to CHC, was used to remove the influence of CO₂-sensitive olfactory chemoreceptors, which inhibit breathing. Exposure to chronic hyperoxic hypercapnia (CHH) was used to reduce the level of arterial chemoreceptor input compared with CHC alone. In vivo experiments examined the effects of CHC, CHH and OD on the acute hypercapnic ventilatory response of intact animals. In vitro, a reduction in artifical cerebral spinal fluid (aCSF) pH increased fictive breathing in preparations taken from control and CHC animals. CHC caused an increase in fictive breathing compared with controls. OD and CHH abolished the CHC-induced augmentation of fictive breathing. In vivo, CHC did not cause an augmentation of the acute hypercapnic ventilatory response. CHH reduced the in vivo acute hypercapnic ventilatory response compared with animals exposed to CHC. In vivo, OD reduced breathing frequency and increased breath amplitude in both control and CHC animals. The results suggest that afferent input from olfactory and arterial chemoreceptors, during CHC, is involved in triggering the CHC-induced increase in central respiratory-related pH/CO₂ chemosensitivity.

Key words: brainstem-spinal cord preparations, central pH/CO₂ chemoreceptors, chronic hypercapnia, chronic hyperoxia, olfactory chemoreceptors