@article{oai:kindai.repo.nii.ac.jp:00020938,
 author = {森島, 真幸 and 藤田, 崇史 and 小野, 克重},
 issue = {53},
 journal = {近畿大学農学部紀要, MEMOIRS OF THE FACULTY OF AGRICULTURE OF KINDAI UNIVERSITY},
 month = {Mar},
 note = {[Synopsis] Brain-derived neurotrophic factor (BDNF), conditionally secreted at active synapse through the stimulation of the tropomyosin-related kinase receptor B (TrkB) receptors, plays an important role in neuronal development, survival, and function. BDNF/TrkB signaling is reportedly essential for organ development or normal contractility in the mammalian heart. However, the expression patterns of BDNF/TrkB and their pathophysiologic roles are poorly understood in the heart. Here we report that BDNF/TrkB signaling is associated with cardiac automaticity in normal and hypoxic conditions. Expressions of BDNF and its receptor TrkB mRNAs in the atrium and the ventricle were abundant, which was approximately a half of those in brainstem or hippocampus, in an age-dependent manner. In hypoxic condition at 3 h (1%,O2), expression of BDNF mRNA was transiently activated in neonatal rat cardiomyocytes (126±7%), whereas this action was reduced (52±2%) at prolonged hypoxia (24 h). Reduction of the cellular automaticity, viability, and T-type Ca2+ channel expression by hypoxia were observed concomitantly with the inactivation of the BDNF/TrkB signal. Our data provide the first evidence that BDNF/TrkB signaling contributes to cardiac dysfunction under acute and prolonged hypoxia., application/pdf},
 pages = {11--23},
 title = {〈原著〉脳由来神経栄養因子BDNFの心臓における発現と低酸素病態下での機能},
 year = {2020},
 yomi = {モリシマ, マサキ and フジタ, タカフミ and オノ, カツシゲ}
}