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Repetitive Acute Intermittent Hypoxia Increases BDNF and TrkB Expression in Respiratory Motor Neurons: Dose Effects
Author(s) -
Satriotomo Irawan,
Vinit Stéphane,
Flom Amy L,
Mitchell Gordon S
Publication year - 2010
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.24.1_supplement.799.16
Subject(s) - tropomyosin receptor kinase b , intermittent hypoxia , hypoxia (environmental) , respiratory system , phrenic nerve , neuroplasticity , medicine , brain derived neurotrophic factor , anesthesia , biology , neuroscience , neurotrophic factors , receptor , chemistry , organic chemistry , oxygen , obstructive sleep apnea
Acute intermittent hypoxia (AIH) initiates respiratory plasticity, including phrenic long‐term facilitation (LTF). pLTF requires new BDNF synthesis and TrkB activation. Repetitive AIH enhances pLTF (Vinit et al., ibid ) via mechanisms of transcriptional regulation modulated by glycolytic flux (MacFarlane et al., ibid ). Distinct models of repetitive AIH elicit pLTF meta‐plasticity, including daily AIH (dAIH: 10 episodes/day, 7 days; 10.5% O2) and thrice weekly AIH (3xwAIH: 10, 5min episodes/day, 3 days per week for 4 or 10 weeks). Here, we tested the hypothesis that these repetitive AIH protocols elicit differential BDNF and TrkB expression in phrenic motor neurons. Semi‐quantitative immunohistochemistry was used to compare BDNF and TrkB expression in presumptive phrenic motor neurons (C4) from rats exposed to dAIH and 3xwAIH for 4 or 10 weeks. BDNF expression was increased by all treatments, although dAIH had less effect vs 3xwAIH; there was no apparent difference between 4 vs 10 weeks 3xwAIH. TrkB expression was also increased, with the larger but equal increases after 4 and 10 weeks of 3xwAIH, and a lesser increase after dAIH. A detailed understanding of repetitive AIH protocols and their relative impact on respiratory plasticity may have important implications in the development of therapeutic strategies for the treatment of clinical disorders with limited ventilatory capacity (NIH NS057778 and HL69064).