ArticleDevelopmental neurobiology2010
Neuroplasticity of the central hypercapnic ventilatory response: teratogen-induced impairment and subsequent recovery during development.
Article in Developmental neurobiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Buccal rhythmogenesis and CORespiratory physiology & neurobiology · 2019Article
- The rostral medulla of bullfrog tadpoles contains critical lung rhythmogenic and chemosensitive regions across metamorphosis.Comparative biochemistry and physiology. Part A, Molecular & integrative physiology · 2018Article
- The cellular building blocks of breathing.Comprehensive Physiology · 2012Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Neuroventilation is highly plastic and exposure to either of two distinct teratogens, nicotine or ethanol, during development results in a similar loss of the neuroventilatory response to hypercapnia in bullfrog tadpoles. Whether this functional deficit is permanent or transient following nicotine or ethanol exposure was unknown. Here, we tested the persistence of hypercapnic neuroventilatory response impairments in tadpoles exposed to either 30 microg/L nicotine or 0.12-0.06 g/dL ethanol for 10 weeks. Brainstem breathing-related neural activity was assessed in tadpoles allowed to develop teratogen-free after either nicotine or ethanol exposure. Nicotine-exposed animals responded normally to hypercapnia after a 3-week teratogen-free period but the hypercapnic response in ethanol-exposed tadpoles remained impaired. Tadpoles allowed to develop for only 1 week nicotine free after chronic exposure were unable to respond to hypercapnia. The hypercapnic response of ethanol-exposed tadpoles returned by 6 weeks following chronic ethanol exposure. These findings suggest that some nicotine- and ethanol-induced impairments can be resolved during early development. Understanding both the disruptive effects of nicotine and ethanol exposure and how impaired responses return when teratogen exposure stops may offer insight on the function and plasticity of respiratory control.
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Registered trials
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