Document Type

Article

Department/Program

Neuroscience

Journal Title

J Neurosci

Pub Date

8-19-2015

Volume

35

Issue

33

Journal Article URL

http://www.jneurosci.org/content/35/33/11606

Abstract

The brainstem preBötzinger complex (preBötC) generates the rhythm underlying inspiratory breathing movements and its core interneurons are derived from Dbx1-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 afferent axonal projections to Dbx1 preBötC neurons undergo activity-dependent depression and we identify a refractory period (∼2 s) after endogenous inspiratory bursts that precludes light-evoked bursts in channelrhodopsin-expressing Dbx1 preBötC neurons. We demonstrate that the duration of the refractory period—but neither the cycle period nor the magnitude of endogenous inspiratory bursts—is sensitive to changes in extracellular Ca2+. Further, we show that postsynaptic factors are unlikely to explain the refractory period or its modulation by Ca2+. Our findings are consistent with the hypothesis that short-term synaptic depression in Dbx1 preBötC neurons influences the inspiratory–expiratory phase transition during respiratory rhythmogenesis.

DOI

https://doi.org/10.1523/JNEUROSCI.0351-15.2015

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