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Calcium and avian intrapulmonary chemoreceptor response to CO₂

S. C. Hempleman,¹ S. X. Egan,^1, J. Q. Pilarski,¹ T. P. Adamson,² and I. C. Solomon³

¹Department of Biological Sciences, Northern Arizona University, Flagstaff, Arizona; ²Division of Neurobiology, Physiology and Behavior, University of California at Davis, Davis, California; and ³Department of Physiology and Biophysics, State University of New York at Stony Brook, Stony Brook, New York

Submitted 24 January 2006 ; accepted in final form 31 July 2006

Intrapulmonary chemoreceptors (IPC) are highly responsive respiratory chemoreceptors that innervate the lungs of birds and diapsid reptiles. IPC are stimulated by low levels of lung PCO₂, inhibited by high levels of lung PCO₂, and their vagal afferents serve as a sensory limb for reflex adjustments of breathing depth and rate. Most IPC exhibit both phasic and tonic sensitivity to CO₂, and spike frequency adaptation (SFA) contributes to their phasic CO₂ responsiveness. To test whether CO₂ responsiveness and SFA in IPC is modulated by a Ca²⁺-linked mechanism, we quantified the role of transmembrane Ca²⁺ fluxes and Ca²⁺-related channels on single-unit IPC function in response to phasic changes in inspired PCO₂. We found that 1) broad-spectrum blockade of Ca²⁺ channels using cadmium or cobalt and blockade of L-type Ca²⁺ channels using nifedipine increased IPC discharge; 2) activation of L-type Ca²⁺ channels using BAY K 8644 reduced IPC discharge; 3) blockade of Ca²⁺-activated potassium channels using charybdotoxin (antagonist of large-conductance Ca²⁺-dependent K⁺ channel) increased IPC discharge, but neither charybdotoxin nor apamin affected SFA; and 4) blockade of chloride channels, including Ca²⁺-activated chloride channels, with niflumic acid decreased IPC discharge at low PCO₂ and increased IPC discharge at high PCO₂, resulting in a net attenuation of the IPC CO₂ response. We conclude that Ca²⁺ influx through L-type Ca²⁺ channels has an inhibitory effect on IPC afferent discharge and CO₂ sensitivity, that spike frequency adaptation is not due to apamin- or charybdotoxin-sensitive Ca²⁺-activated K⁺ channels in IPC, and that chloride channels blocked by niflumic acid help modulate IPC CO₂ responses.

signal transduction; intracellular pH; spike frequency adaptation; lung; vagus