ArticleRespiratory physiology & neurobiology2015
Changes in carotid body and nTS neuronal excitability following neonatal sustained and chronic intermittent hypoxia exposure.
Article in Respiratory physiology & neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Perinatal Hypoxemia and Oxygen Sensing.Comprehensive Physiology · 2021Article
- Acute lung injury in neonatal rats causes postsynaptic depression in nucleus tractus solitarii second-order neurons.Respiratory physiology & neurobiology · 2019Article
- Combined effects of intermittent hyperoxia and intermittent hypercapnic hypoxia on respiratory control in neonatal rats.Respiratory physiology & neurobiology · 2019Article
- Loss ofeLife · 2018Article
- Respiratory dysfunction following neonatal sustained hypoxia exposure during a critical window of brain stem extracellular matrix formation.American journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
- Cardiorespiratory events in preterm infants: etiology and monitoring technologies.Journal of perinatology : official journal of the California Perinatal Association · 2016Review
- Chronic intermittent hyperoxia alters the development of the hypoxic ventilatory response in neonatal rats.Respiratory physiology & neurobiology · 2016Article
- Oxygen extremes, inflammation, and neonatal breathing.Respiratory physiology & neurobiologyReview
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
We investigated whether pre-treatment with neonatal sustained hypoxia (SH) prior to chronic intermittent hypoxia (SH+CIH) would modify in vitro carotid body (CB) chemoreceptor activity and the excitability of neurons in the caudal nucleus of the solitary tract (nTS). Sustained hypoxia followed by CIH exposure simulates an oxygen paradigm experienced by extremely premature infants who developed persistent apnea. Rat pups were treated with 5 days of SH (11% O2) from postnatal age 1 (P1) followed by 10 days of subsequent chronic intermittent hypoxia (CIH, 5% O2/5 min, 8 h/day, between P6 and P15) as described previously (Mayer et al., Respir. Physiol. Neurobiol. 187(2): 167-75, 2013). At the end of SH+CIH exposure (P16), basal firing frequency was enhanced, and the hypoxic sensory response of single unit CB chemoafferents was attenuated. Further, basal firing frequency and the amplitude of evoked excitatory post-synaptic currents (ESPC's) of nTS neurons was augmented compared to age-matched rats raised in normoxia. These effects were unique to SH+CIH exposure as neither SH or CIH alone elicited any comparable effect on chemoafferent activity or nTS function. These data indicated that pre-treatment with neonatal SH prior to CIH exposure uniquely modified mechanisms of peripheral (CB) and central (nTS) neural function in a way that would be expected to disturb the ventilatory response to acute hypoxia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.