Reduced respiratory neural activity elicits phrenic motor facilitation |
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Authors: | Mahamed Safraaz Strey Kristi A Mitchell Gordon S Baker-Herman Tracy L |
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Affiliation: | a Department of Comparative Biosciences, University of Wisconsin (Madison), 2015 Linden Drive, Madison, WI 53706-1102, USA |
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Abstract: | We hypothesized that reduced respiratory neural activity elicits compensatory mechanisms of plasticity that enhance respiratory motor output. In urethane-anesthetized and ventilated rats, we reversibly reduced respiratory neural activity for 25-30 min using: hypocapnia (end tidal CO(2)=30 mmHg), isoflurane (~1%) or high frequency ventilation (HFV; ~100 breaths/min). In all cases, increased phrenic burst amplitude was observed following restoration of respiratory neural activity (hypocapnia: 92±22%; isoflurane: 65±22%; HFV: 54±13% baseline), which was significantly greater than time controls receiving the same surgery, but no interruptions in respiratory neural activity (3±5% baseline, p<0.05). Hypocapnia also elicited transient increases in respiratory burst frequency (9±2 versus 1±1bursts/min, p<0.05). Our results suggest that reduced respiratory neural activity elicits a unique form of plasticity in respiratory motor control which we refer to as inactivity-induced phrenic motor facilitation (iPMF). iPMF may prevent catastrophic decreases in respiratory motor output during ventilatory control disorders associated with abnormal respiratory activity. |
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Keywords: | Hypocapnia Isoflurane Activity deprivation Inactivity Respiratory control Phrenic motor facilitation Homeostatic plasticity Control of breathing Phrenic plasticity Reduced neural activity |
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