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The Journal of Neuroscience, July 15, 2001, 21(14):5381-5388

Chronic Intermittent Hypoxia Elicits Serotonin-Dependent Plasticity in the Central Neural Control of Breathing

Liming Ling1, David D. Fuller1, Karen B. Bach1, Richard Kinkead1, E. Burdette Olson Jr2, and Gordon S. Mitchell1

1 Departments of Comparative Biosciences and 2 Preventive Medicine, University of Wisconsin, Madison, Wisconsin 53706

We tested the hypothesis that chronic intermittent hypoxia (CIH) elicits plasticity in the central neural control of breathing via serotonin-dependent effects on the integration of carotid chemoafferent inputs. Adult rats were exposed to 1 week of nocturnal CIH (11-12% O2/air at 5 min intervals; 12 hr/night). CIH and untreated rats were then anesthetized, paralyzed, vagotomized, and artificially ventilated. Time-dependent hypoxic responses were assessed in the phrenic neurogram during and after three 5 min episodes of isocapnic hypoxia. Integrated phrenic amplitude (int Phr) responses during hypoxia were greater after CIH at arterial oxygen pressures (PaO2) between 25 and 45 mmHg (p < 0.05), but not at higher PaO2 levels. CIH did not affect hypoxic phrenic burst frequency responses, although the post-hypoxia frequency decline that is typical in rats was abolished. int Phr and frequency responses to electrical stimulation of the carotid sinus nerve were enhanced by CIH (p < 0.05). Serotonin-dependent long-term facilitation (LTF) of int Phr was enhanced after CIH at 15, 30, and 60 min after episodic hypoxia (p < 0.05). Pretreatment with the serotonin receptor antagonists methysergide (4 mg/kg, i.v.) and ketanserin (2 mg/kg, i.v.) reversed CIH-induced augmentation of the short-term hypoxic phrenic response and restored the post-hypoxia frequency decline in CIH rats. Whereas methysergide abolished CIH-enhanced phrenic LTF, the selective 5-HT2 antagonist ketanserin only partially reversed this effect. The results suggest that CIH elicits unique forms of serotonin-dependent plasticity in the central neural control of breathing. Enhanced LTF after CIH may involve an upregulation of a non-5-HT2 serotonin receptor subtype or subtypes.

Key words: control of breathing; serotonin; plasticity; hypoxia; phrenic motoneurons; rats

Copyright © 2001 Society for Neuroscience  0270-6474/01/21145381-08$05.00/0


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