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Inactivity‐induced phrenic motor facilitation is associated with decreased phrenic burst‐to‐burst variability
Author(s) -
Borchert Corie,
Strey Kristi A,
Baertsch Nathan,
Baker-Herman Tracy L
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1148.4
Subject(s) - phrenic nerve , apnea , anesthesia , medicine , respiratory system
Reduced respiratory neural activity in ventilated rats elicits rebound increases in phrenic discharge once neural activity has been restored, a form of plasticity called inactivity‐induced phrenic motor facilitation (iPMF). We hypothesized that iPMF is associated with reduced phrenic burst‐to‐burst variability. Phrenic discharge was measured in anesthetized, vagotomized and ventilated Harlan (H) and Charles River (CR) Sprague Dawley rats exposed to a 30 min neural apnea or an equal duration of baseline conditions (time control). As expected, H rats expressed iPMF at 5 and 60 (p<0.05) min post‐apnea, whereas CR rats expressed iPMF only at 5 (p<0.05), but not 60 (p>0.05) min. Inspiratory time (Ti), expiratory time (Te) and peak area variability was assessed using Poincare plot analyses for burst n vs burst n+1 before, and 5 and 60 min post‐apnea. In H rats exposed to a neural apnea, standard deviations of the Poincare plot (SD1, SD2) for Ti and Te were significantly decreased at 5 and 60 min post‐apnea (p< 0.01). In CR rats exposed to a neural apnea, decreases in SD1 and SD2 for Ti and Te were observed at 5 (p<0.01), but not 60 (p>0.05) min post‐apnea. No changes in SD1 or SD2 for Ti or Te were observed in time controls (p>0.05), and no changes in SD1 or SD2 for peak area were observed in any group (p>0.05). These data suggest that iPMF is associated with decreased variability in Ti and Te. NIH HL105511 and UW‐Madison Regent Scholars Fund