Abstract
Interneurons derived from Dbx1-expressing precursors located in the brainstem preBötzinger complex (preBötC) putatively form the core oscillator for inspiratory breathing movements. We tested this Dbx1 core hypothesis by expressing archaerhodopsin in Dbx1-derived interneurons and then transiently hyperpolarizing these neurons while measuring respiratory rhythm in vitro or breathing in vagus-intact adult mice. Transient illumination of the preBötC interrupted inspiratory rhythm in both slice preparations and sedated mice. In awake mice, light application reduced breathing frequency and prolonged the inspiratory duration. Support for the Dbx1 core hypothesis previously came from embryonic and perinatal mouse experiments, but these data suggest that Dbx1-derived preBötC interneurons are rhythmogenic in adult mice too. The neural origins of breathing behavior can be attributed to a localized and genetically well-defined interneuron population.
Highlights
Central pattern generator (CPG) networks produce neural activity that underlies rhythmic motor behaviors such as walking, swimming, chewing, and breathing
Whereas Dbx1-derived interneurons were previously studied in the context of embryonic and early neonatal development, these results provide additional evidence that Dbx1 preBötzinger Complex (preBötC) neurons are rhythmogenic in adult mice as well
According to the Dbx1 core hypothesis, interneurons derived from Dbx1-expressing precursors comprise the CPG for inspiratory breathing movements
Summary
Central pattern generator (CPG) networks produce neural activity that underlies rhythmic motor behaviors such as walking, swimming, chewing, and breathing. The CPG for inspiratory breathing movements resides in the preBötzinger Complex (preBötC) of the ventral medulla [1,2], but its cellular composition in adult mammals remains incompletely understood. Silencing or killing peptide and peptide receptor-expressing neurons causes severe respiratory pathology as well as long-lasting apnea in adult rats [4,9,10]. Excitatory synaptic communication mediated by AMPA receptors is essential for rhythmogenesis and respiratory motor output in in vitro breathing models [11,12]. Mice lacking the vesicular glutamate transporter VGLUT2 fail to breathe, even though the preBötC forms, because its constituent rhythmogenic neurons do not activate and synchronize [8]
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