Respiratory plasticity: differential actions of continuous and episodic hypoxia and hypercapnia.
The objectives of this paper are: (1) to review advances in our understanding of the mechanisms of respiratory plasticity elicited by episodic versus continuous hypoxia in short to intermediate time domains (min to h); and (2) to present new data suggesting that different patterns of hypercapnia also elicit distinct forms of respiratory plasticity. Episodic, but not continuous hypoxia elicits long-term facilitation (LTF) of respiratory motor output. Phrenic LTF is a serotonin-dependent central neural mechanism that requires: (a) activation of spinal serotonin receptors; and (b) spinal protein synthesis. Continuous and episodic hypercapnia also elicit different mechanisms of plasticity. Continuous, severe hypercapnia (25 min of approximately 10% inspired CO(2)) elicits long-term depression (LTD) of phrenic motor output (-33+/-8% at 60 min post-hypercapnia) in anesthetized rats. In contrast, 3,5 min hypercapnic episodes do not elicit LTD (9+/-17% at 60 min). We hypothesize that the response of respiratory motoneurons to serotonergic and noradrenergic modulation may contribute to pattern sensitivity to hypoxia and hypercapnia.
Baker
T L
TL
Center for Neuroscience, University of Wisconsin, 2015 Linden Drive West, Madison, WI 53706, USA. BakerT@svm.vetmed.wisc.edu
Fuller
D D
DD
Zabka
A G
AG
Mitchell
G S
GS
D000818:Animals; D002628:Chemoreceptor Cells / Q000503:physiopathology; D006801:Humans; D006935:Hypercapnia / Q000503:physiopathology*; D000860:Hypoxia / Q000503:physiopathology*; D009046:Motor Neurons / Q000502:physiology; D009473:Neuronal Plasticity; D012137:Respiratory System / Q000294:innervation*