Opioids cause hyperpolarization and pre-synaptic suppression among a subset of preBötzinger Complex neurons to impair respiratory rhythmogenesis.

Inspiratory rhythmogenesis is mediated by an emergent mechanism independent of bursts associated with motor output and is modulated by opioids, pointing to strategies for ameliorating opioid-induced respiratory depression.

The neuromodulator substance P enhances mechanisms of recurrent excitation between breaths to control breathing frequency and stability.

Pacemaker neurons are present in the preBötC circuitry of mouse embryos and their role in driving respiratory network activity changes during the critical period immediately before birth.

The predictive power of a computational model advances understanding of the neuronal and circuit biophysical mechanisms that generate the respiratory rhythm and neural activity patterns in the mammalian brainstem.

Functional and anatomical analysis reveal a crucial role played during embryonic development by microglia in the ontogenesis and function of central circuits responsible for respiratory rhythmogenesis.

Laser-ablating neurons of a single genetic class reveals that Dbx1-derived interneurons comprise core respiratory rhythmogenic and premotor circuits and provides quantitative cellular parameters that govern network functionality

Computational modeling motivated by recent experiments clarifies biophysical mechanisms generating the rhythm and amplitude of breathing at the level of neurons and brain circuits in mammals.

Electrophysiological analyses reveal interactions between gasotransmitter enzymes and their respective products that regulate hypoglossal motoneuron excitability and may drive changes in upper airway tone in obstructive sleep apnea and perturb behaviors such as vocalization and swallowing.

Computational models are helping researchers to understand how certain properties of neurons contribute to respiratory rhythms.