Photostimulation of NTS Phox2b neurons projecting to the preBötC amplified baseline ventilation, whereas their genetic ablation blunted CO2-stimulated ventilatory responses.
Identifies a specific medullary network involving NTS and preBötC neurons that integrates chemosensory feedback to control respiratory homeostasis.
Abstract The dynamic interaction between central respiratory chemoreceptors and the respiratory central pattern generator constitutes a critical homeostatic axis for stabilizing breathing rhythm and pattern, yet its circuit‐level organization remains poorly characterized. Here, the functional connectivity between two key medullary hubs: the nucleus tractus solitarius (NTS) and the preBötzinger complex (preBötC) are systematically investigated. These findings delineate a medullary network primarily comprising Phox2b‐expressing NTS neurons (NTS Phox2b ), GABAergic NTS neurons (NTS GABA ), and somatostatin (SST)‐expressing preBötC neurons (preBötC SST ). Photostimulation of NTS Phox2b neurons projecting to the preBötC potently amplifies baseline ventilation, whereas genetic ablation of these neurons or knockout of their transient receptor potential channel 5 (TRPC5) significantly blunts the CO 2 ‐stimulated ventilatory responses. Conversely, NTS GABA neuron stimulation inhibits or halts breathing partially via monosynaptic inhibition of NTS Phox2b neurons projecting to the preBötC. Additionally, photostimulation of preBötC SST neurons projecting to the NTS drives deep and slow breathing through coordinated modulation of NTS GABA and NTS Phox2b neurons. These findings collectively identify an important medullary network that integrates chemosensory feedback with respiratory motor output, enabling dynamic tuning of breathing patterns to metabolic demands.
Deng et al. (Sun,) reported a other. Photostimulation and genetic ablation of medullary neurons was evaluated on Ventilatory responses. Photostimulation of NTS Phox2b neurons projecting to the preBötC amplified baseline ventilation, whereas their genetic ablation blunted CO2-stimulated ventilatory responses.