Chronic hyperoxia alters the expression of neurotrophic factors in the carotid body of neonatal rats

• Published in: Respiratory physiology & neurobiology 2011-02, Vol.175 (2), p.220-227
• Main Authors: Dmitrieff, Elizabeth F, Wilson, Julia T, Dunmire, Kyle B, Bavis, Ryan W
• Format: Article
• Language: English
• Subjects: Animals; Animals, Newborn; Biological and medical sciences; Carotid Body - metabolism; Control of breathing; Fundamental and applied biological sciences. Psychology; Glial Cell Line-Derived Neurotrophic Factor Receptors - metabolism; Hyperoxia - metabolism; Medical Education; mRNA expression; Nerve Growth Factors - metabolism; Neuroplasticity; Neurotrophin; Peripheral chemoreceptor; Protein expression; Pulmonary/Respiratory; Rats; Rats, Sprague-Dawley; Receptor Protein-Tyrosine Kinases - metabolism; Receptor, trkB - metabolism; Vertebrates: respiratory system
• ISSN: 1569-9048; 1878-1519
• DOI: 10.1016/j.resp.2010.11.007

Abstract Chronic exposure to hyperoxia alters the postnatal development and innervation of the rat carotid body. We hypothesized that this plasticity is related to changes in the expression of neurotrophic factors or related proteins. Rats were reared in 60% O2 from 24 to 36 h prior to birth until studied at 3 d of age (P3). Protein levels for brain-derived neurotrophic factor (BDNF) were significantly reduced (−70%) in the P3 carotid body, while protein levels for its receptor, tyrosine kinase B, and for glial cell line-derived neurotrophic factor (GDNF) were unchanged. Transcript levels in the carotid body were downregulated for the GDNF receptor Ret (−34%) and the neuropeptide Vgf (−67%), upregulated for Cbln1 (+205%), and unchanged for Fgf2; protein levels were not quantified for these genes. Immunohistochemical analysis revealed that Vgf and Cbln1 proteins are expressed within the carotid body glomus cells. These data suggest that BDNF, and perhaps other neurotrophic factors, contribute to abnormal carotid body function following perinatal hyperoxia.