Chronic intermittent hypoxia elicits serotonin-dependent plasticity in the central neural control of breathing.

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