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Neuroanatomical and neurophysiological evidence of pulmonary nociceptor and carotid chemoreceptor convergence in the nucleus tractus solitarius and nucleus ambiguus

Pulmonary vagal nociceptors defend the airways. Cardiopulmonary vagal nociceptors synapse in the nucleus tractus solitarius (NTS). Evidence has demonstrated the convergence of cardiopulmonary nociceptors with afferents from carotid chemoreceptors. Whether sensory convergence occurs in motor nuclei a...

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Detalles Bibliográficos
Autores principales: Zyuzin, Jekaterina, Jendzjowsky, Nicholas
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Physiological Society 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9142158/
https://www.ncbi.nlm.nih.gov/pubmed/35443145
http://dx.doi.org/10.1152/jn.00125.2022
Descripción
Sumario:Pulmonary vagal nociceptors defend the airways. Cardiopulmonary vagal nociceptors synapse in the nucleus tractus solitarius (NTS). Evidence has demonstrated the convergence of cardiopulmonary nociceptors with afferents from carotid chemoreceptors. Whether sensory convergence occurs in motor nuclei and how sensory convergence affects reflexive efferent motor output directed toward the airways are critical knowledge gaps. Here, we show that distinct tracer injection into the pulmonary nociceptors and carotid chemoreceptors leads to co-labeled neurons in the nucleus tractus solitarius and nucleus ambiguus. Precise simultaneous stimulation delivered to pulmonary nociceptors and carotid chemoreceptors doubled efferent vagal output, enhanced phrenic pause, and subsequently augmented phrenic motor activity. These results suggest that multiple afferents are involved in protecting the airways and concurrent stimulation enhances airway defensive reflex output. NEW & NOTEWORTHY Sensory afferents have been shown to converge onto nucleus tractus solitarius primary neurons. Here, we show sensory convergence of two distinct sets of sensory afferents in motor nuclei of the nucleus ambiguus, which results in augmentation of airway defense motor output.