Acute perturbation of Pet1-neuron activity in neonatal mice impairs cardiorespiratory homeostatic recovery.
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ABSTRACT: Cardiorespiratory recovery from apneas requires dynamic responses of brainstem circuitry. One implicated component is the raphe system of Pet1-expressing (largely serotonergic) neurons, however their precise requirement neonatally for homeostasis is unclear, yet central toward understanding newborn cardiorespiratory control and dysfunction. Here we show that acute in vivo perturbation of Pet1-neuron activity, via triggering cell-autonomously the synthetic inhibitory receptor hM4Di, resulted in altered baseline cardiorespiratory properties and diminished apnea survival. Respiratory more than heart rate recovery was impaired, uncoupling their normal linear relationship. Disordered gasp recovery from the initial apnea distinguished mice that would go on to die during
SUBMITTER: Dosumu-Johnson RT
PROVIDER: S-EPMC6199134 | biostudies-literature | 2018 Oct
REPOSITORIES: biostudies-literature
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