The central network controlling breathing exhibits plasticity in response to environmental challenges, such as chronic intermittent hypoxia (CIH). For a better understanding of the effects of CIH on the central generation of breathing, we combined single cell qRT-PCR, nerve and whole cell patch clamp recordings of Bötzinger Complex (BötC) and pre-Bötzinger Complex (pre-BötC) respiratory neurons in in situ preparations from control and CIH rats. In the BötC, we recorded 32 augmenting-expiratory (aug-E; glicinergic) and 24 post-inspiratory (post-I; 19 glicinergic and 5 glutamatergic) neurons, which present distinct intrinsic electrophysiological properties. CIH decreased the superior laryngeal nerve (SLN) post-inspiratory activity, by increasing potassium-mediated leak current in the post-I neurons, and increased the duration of expiration by changes in the aug-E neurons. In the pre-BötC, we recorded four types of neurons: pre-inspiratory (pre-I; 15 glutamatergic, 9 GABAergic and 11 glicinergic), early-inspiratory (19 glicinergic neurons), ramp-inspiratory (13 glicinergic and 9 GABAergic) and late-inspiratory (7 GABAergic and 9 glicinergic). CIH enhanced SLN pre-I activity, by increasing the inward riluzole-sensitive persistent sodium current in the intrinsically bursting glutamatergic pre-I neurons. These data show that CIH triggers a reconfiguration of synaptic interaction within the respiratory network in rats, which seems to be an adaptive process required for appropriated pulmonary ventilation and regulation of upper airway resistance. Support: FAPESP, CAPES and CNPQ.