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Published on: March 14, 2012
Calcium and avian intrapulmonary chemoreceptor response to CO2
S C Hempleman1, S X Egan, J Q Pilarski
11Department of Biological Sciences, Northern Arizona University, Flagstaff, Arizona 86011-5640, USA. steven.hempleman@nau.edu
Calcium influx via L-type channels inhibits intrapulmonary chemoreceptors (IPC) in reptiles and birds. Chloride channels modulate IPC responses to carbon dioxide, impacting breathing regulation.
Area of Science:
- Comparative Physiology
- Respiratory Neurobiology
- Chemoreception
Background:
- Intrapulmonary chemoreceptors (IPC) in birds and reptiles are vital for respiratory control.
- IPC exhibit sensitivity to carbon dioxide (CO2) and spike frequency adaptation (SFA).
- The role of calcium (Ca2+) in modulating IPC function and CO2 responsiveness is not fully understood.
Purpose of the Study:
- To investigate the influence of transmembrane Ca2+ fluxes and Ca2+-related channels on IPC function.
- To determine if Ca2+ mechanisms modulate CO2 responsiveness and SFA in single-unit IPC.
- To elucidate the specific roles of L-type Ca2+ channels, Ca2+-activated K+ channels, and chloride channels.
Main Methods:
- Single-unit electrophysiological recordings from avian IPC.
- Pharmacological manipulation using channel blockers (cadmium, cobalt, nifedipine, charybdotoxin, apamin, niflumic acid) and activators (BAY K 8644).
- Assessment of IPC discharge and spike frequency adaptation (SFA) under varying inspired Pco2 conditions.
Main Results:
- Blockade of Ca2+ channels (Cd2+, Co2+, nifedipine) increased IPC discharge; L-type Ca2+ channel activation (BAY K 8644) decreased it, indicating an inhibitory Ca2+ influx.
- Blockade of Ca2+-activated K+ channels (charybdotoxin, apamin) increased IPC discharge but did not affect SFA.
- Blockade of chloride channels (niflumic acid) attenuated the IPC CO2 response by reducing discharge at low Pco2 and increasing it at high Pco2.
Conclusions:
- Ca2+ influx through L-type Ca2+ channels exerts an inhibitory effect on IPC afferent discharge and CO2 sensitivity.
- Spike frequency adaptation in IPC is not mediated by apamin- or charybdotoxin-sensitive Ca2+-activated K+ channels.
- Chloride channels, targeted by niflumic acid, play a significant role in modulating IPC CO2 responses.
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