The control of breathing in birds with particular reference to the initiation and maintenance of diving apnea.
Avian respiratory pacemaker activity is dependent on some form of peripheral input but it may be inhibited by both central and peripheral stimulation. At present the results of central nervous stimulation are difficult to interpret but, aside from cortical influences, diving apnea appears to be maintained, in the face of increasing chemoreceptor input, by noxious stimulation of the upper respiratory tract and depression of the output of medullary respiratory neurons by advancing hypercapnia. If this is so, an obvious problem for future research is what initiates the prompt onset of hyperpnea when the animal surfaces and breathes. It is known that post-dive hyperpnea is little affected by either carotid body or pulmonary denervation, so peripheral chemoreceptors are unlikely to play a major role in this response.
D000200:Action Potentials; D000818:Animals; D001049:Apnea / Q000503:physiopathology*; D001158:Arteries / Q000294:innervation; D001717:Birds / Q000502:physiology*; D001794:Blood Pressure; D001921:Brain / Q000502:physiology*; D002245:Carbon Dioxide / Q000494:pharmacology; D002628:Chemoreceptor Cells / Q000502:physiology; D004242:Diving; D006339:Heart Rate; D008168:Lung / Q000294:innervation / Q000502:physiology; D008465:Mechanoreceptors / Q000502:physiology; D009142:Musculoskeletal Physiological Phenomena; D009474:Neurons / Q000502:physiology; D011434:Proprioception; D012018:Reflex; D012119:Respiration / Q000187:drug effects; D012143:Respiratory Physiological Phenomena; D014630:Vagus Nerve / Q000502:physiology
D002245:Carbon Dioxide