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Does reduced carotid body BDNF contribute to developmental hyperoxia‐induced respiratory plasticity?
Author(s) -
Muscato Gwen M.,
Kim Maria S.,
McDonough Amy B.,
Bavis Ryan W.
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.1055.3
Subject(s) - hyperoxia , carotid body , tropomyosin receptor kinase b , hypoxic ventilatory response , brain derived neurotrophic factor , neurotrophic factors , medicine , endocrinology , agonist , hypoxia (environmental) , anesthesia , neuroplasticity , developmental plasticity , respiratory system , receptor , chemistry , lung , electrophysiology , plasticity , physics , organic chemistry , psychiatry , oxygen , thermodynamics
Chronic exposure to moderate hyperoxia (60% O 2 ) reduces carotid body expression of brain‐derived neurotrophic factor (BDNF) in neonatal rats. Reduced BDNF expression correlates with abnormal carotid body development and blunted hypoxic ventilatory responses, but a causal relationship has not been established. First, we used ELISA to confirm that both sustained and intermittent exposures to 60% O 2 reduced carotid body BDNF levels; intermittent hypercapnic hypoxia had the opposite effect. Next, we attempted to block the effects of developmental hyperoxia by administering LM22A4 (50 mg kg −1 , i.p., daily), an agonist for BDNF's TrkB receptor. After 7 days of treatment with 60% O 2 , carotid body volume and the hypoxic ventilatory response were significantly reduced in P7 rats that received either LM22A4 or vehicle (saline) from birth; the drug treatment did not attenuate this effect. Similar results were obtained using an alternate TrkB agonist, 7,8‐dihydroxyflavone (5 mg kg −1 , i.p., daily). Although carotid body BDNF expression appears to be regulated by environmental O 2 , our data do not support the hypothesis that reduced BDNF is directly responsible for hyperoxia‐induced developmental plasticity in respiratory control. Support or Funding Information Supported by NIH grant R15 HL‐114001.