Journal Article URL
The brainstem pre-Botzinger complex (preBotC) generates the rhythm underlying inspiratory breathing movements and its core interneurons are derived from Dbx-1 expressing precursors. Recurrent synaptic excitation is required to initiate inspiratory bursts, but whether excitatory synaptic mechanisms also contribute to inspiratory–expiratory phase transition is unknown. Here, we examined the role of short-term synaptic depression using a rhythmically active neonatal mouse brainstem slice preparation. We show that different axonal projections to Dbx-1 PreBotC neurons undergo activity-dependent depression and we identify a refractory period (approx. 2 s) after endogenous inspiratory bursts that precludes light-evoked bursts in channelrhodopsin-expressing Dbx1 Pre-BotC neurons. We demonstrate that the duration of the refractory period---but neither the cycle period nor the magnitude of endogenous inspiratory burst---is sensitive to changes in extracellular Ca^2+. Further, we show that postsynaptic factors are unlikely to explain the refractory period or its modulation by Ca^2+. Our findings are consistent with the hypothesis that short-term synaptic depression in Dbx-1 Pre-BotC neurons influences the inspiratory-expiratory phase transition during respiratory rhythmogenesis.
Song, Hanbing; Hayes, John A.; Vann, Nicolas A.; LaMar, M. Drew; and Del Negro, Christopher A., Mechanisms Leading to Rhythm Cessation in the Respiratory PreBotzinger Complex Due to Piecewise Cumulative Neuronal Deletions (2015). eNeuro, 2(4).
A correction to this article was made in 2016.
Correction- Correction Mechanisms Leading to Rhythm Cessation in the Respiratory PreBötzinger Complex Due to Piecewise Cumulative Neuronal Deletions