title: Reduced respiratory neural activity elicits a long-lasting decrease in the CO2threshold for apnea in anesthetized rats.
abstract: Two critical parameters that influence breathing stability are the levels of arterial pCO2at which breathing ceases and subsequently resumes - termed the apneic and recruitment thresholds (AT and RT, respectively). Reduced respiratory neural activity elicits a chemoreflex-independent, long-lasting increase in phrenic burst amplitude, a form of plasticity known as inactivity-induced phrenic motor facilitation (iPMF). The physiological significance of iPMF is unknown. To determine if iPMF and neural apnea have long-lasting physiological effects on breathing, we tested the hypothesis that patterns of neural apnea that induce iPMF also elicit changes in the AT and RT. Phrenic nerve activity and end-tidal CO2were recorded in urethane-anesthetized, ventilated rats to quantify phrenic nerve burst amplitude and the AT and RT before and after three patterns of neural apnea that differed in their duration and ability to elicit iPMF: brief intermittent neural apneas, a single brief "massed" neural apnea, or a prolonged neural apnea. Consistent with our hypothesis, we found that patterns of neural apnea that elicited iPMF also resulted in changes in the AT and RT. Specifically, intermittent neural apneas progressively decreased the AT with each subsequent neural apnea, which persisted for at least 60min. Similarly, a prolonged neural apnea elicited a long-lasting decrease in the AT. In both cases, the magnitude of the AT decrease was proportional to iPMF. In contrast, the RT was transiently decreased following prolonged neural apnea, and was not proportional to iPMF. No changes in the AT or RT were observed following a single brief neural apnea. Our results indicate that the AT and RT are differentially altered by neural apnea and suggest that specific patterns of neural apnea that elicit plasticity may stabilize breathing via a decrease in the AT.
authors.affiliation: Department of Comparative Biosciences, University of Wisconsin-Madison, 2015 Linden Drive, Madison, WI 53706, USA.
authors.forename: N A
authors.initials: NA
authors.lastname: Baertsch
authors.affiliation: Department of Comparative Biosciences, University of Wisconsin-Madison, 2015 Linden Drive, Madison, WI 53706, USA. Electronic address: bakert@svm.vetmed.wisc.edu.
authors.forename: T L
authors.initials: TL
authors.lastname: Baker
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000704:Analysis of Variance; D000758:Anesthesia; D000818:Animals; D001049:Apnea / Q000473:pathology / Q000503:physiopathology*; D001784:Blood Gas Analysis; D001794:Blood Pressure / Q000187:drug effects; D002245:Carbon Dioxide / Q000378:metabolism* / Q000494:pharmacology; D004195:Disease Models, Animal; D008297:Male; D009046:Motor Neurons / Q000187:drug effects / Q000502:physiology*; D010791:Phrenic Nerve / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012684:Sensory Thresholds / Q000502:physiology*; D013997:Time Factors
chemical_list: D002245:Carbon Dioxide
keywords: Apnea; Apneic threshold; CSA; Central sleep apnea; Chemoreflex; Control of breathing; Phrenic; Plasticity; Reduced respiratory neural activity; Respiratory motor neurons; iPMF