1. The pre-Bötzinger complex (PreBötC) generates different inspiratory rhythms. Under control normoxic conditions, a mixture of intrinsic and synaptic properties underlies the generation of eupnoea by the PreBötC. Under hypoxia, those network properties change and modify the respiratory rhythm pattern. Hypoxia can be caused by a reduction in oxygen availability in the environment, inadequate oxygen transport, an inability of tissues to use oxygen or several pathological conditions.
2. During severe hypoxia, the network properties within the PreBötC are reconfigured whereby the network no longer generates eupnoea, but instead generates a new rhythm, named gasping. Such reconfiguration includes changes in synaptic and intrinsic properties triggered by hypoxia itself, as well as the influence of different neuromodulators released during hypoxia. Gasping has been considered an important arousal mechanism that triggers autoresuscitation. Dysregulation of gasping has been proposed to result in failure to autoresuscitate and has been hypothesised to contribute to Sudden Infant Death Syndrome.
3. Precisely which synaptic and/or neuronal intrinsic membrane properties are critical to central respiratory rhythmogenesis, in either normoxia or hypoxia, is still the subject of considerable debate. In the present article I review how hypoxia alters the respiratory network and discuss my hypotheses regarding the cellular and network mechanisms involved in gasping rhythm generation. Finally, I review changes in the hypoxic response during postnatal development and the contribution of several neuromodulators to such a response.