PMID- 30121216 OWN - NLM STAT- MEDLINE DCOM- 20190307 LR - 20200930 IS - 1872-7972 (Electronic) IS - 0304-3940 (Linking) VI - 685 DP - 2018 Oct 15 TI - Sympathetic nervous remodeling is induced in the intermediolateral nucleus after myocardial infarction - Role of BDNF-TrkB axis. PG - 114-123 LID - S0304-3940(18)30534-2 [pii] LID - 10.1016/j.neulet.2018.08.004 [doi] AB - Several studies have shown that neural remodeling in stellate ganglia (SG) is induced by myocardial infarction (MI). It remains unclear whether neural remodeling after MI is limited in SG within the sympathetic nervous system (SNS). MI was induced in a rat model by ligation of the left anterior descending artery. Neural remodeling in the intermediolateral nucleus (IML) and SG was assessed by immunohistochemistry 2 weeks after MI. The mRNA and protein expressions of brain-derived neurotrophic factor (BDNF), tropomyosin-related kinase receptor (TrkB) and extracellular signal-regulated kinase (ERK) were measured by quantitative RT-PCR, immunohistochemistry and Western blotting 1 week after MI. The neuronal size and axonal density of IML were increased after MI compared to sham. The density of growth-associated protein-43, a protein upregulated in axons undergoing nerve sprouting, was increased after MI compared to sham. The fluorescence intensity of BDNF and TrkB in IML were significantly higher in the MI group than in the sham group. In addition, mRNA expressions of BDNF and TrkB in the spinal cord at the Th2 level was increased after MI. Finally, the percentage of phospho-ERK-immunoreactive cells in IML was significantly higher in the MI group than in the sham group. In conclusion, neural remodeling after MI in IML is associated with the activation of BDNF-TrkB axis. Morphological remodeling throughout the SNS may be involved in sustained activation of sympathetic tone after MI. CI - Copyright (c) 2018 Elsevier B.V. All rights reserved. FAU - Nodera, Minoru AU - Nodera M AD - Department of Cardiovascular Medicine, Fukushima Medical University, Fukushima, Japan. FAU - Oikawa, Masayoshi AU - Oikawa M AD - Department of Cardiovascular Medicine, Fukushima Medical University, Fukushima, Japan. Electronic address: moikawa@fmu.ac.jp. FAU - Nakazato, Kazuhiko AU - Nakazato K AD - Department of Cardiovascular Medicine, Fukushima Medical University, Fukushima, Japan. FAU - Ishida, Takafumi AU - Ishida T AD - Department of Cardiovascular Medicine, Fukushima Medical University, Fukushima, Japan. FAU - Takeishi, Yasuchika AU - Takeishi Y AD - Department of Cardiovascular Medicine, Fukushima Medical University, Fukushima, Japan. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20180816 PL - Ireland TA - Neurosci Lett JT - Neuroscience letters JID - 7600130 RN - 0 (Brain-Derived Neurotrophic Factor) RN - EC 2.7.10.1 (Ntrk2 protein, rat) RN - EC 2.7.10.1 (Receptor, trkB) SB - IM MH - Animals MH - Axons/metabolism MH - Brain-Derived Neurotrophic Factor/*metabolism MH - Male MH - Myocardial Infarction/*metabolism MH - Neurons/metabolism MH - Rats, Sprague-Dawley MH - Receptor, trkB/*metabolism MH - Spinal Cord/metabolism MH - Spinal Cord Lateral Horn/*metabolism MH - Sympathetic Nervous System/metabolism OTO - NOTNLM OT - Brain-derived neurotrophic factor OT - Intermediolateral nucleus OT - Myocardial infarction OT - Neural remodeling OT - Tropomyosin-related kinase receptor B EDAT- 2018/08/20 06:00 MHDA- 2019/03/08 06:00 CRDT- 2018/08/20 06:00 PHST- 2018/03/27 00:00 [received] PHST- 2018/07/06 00:00 [revised] PHST- 2018/08/05 00:00 [accepted] PHST- 2018/08/20 06:00 [pubmed] PHST- 2019/03/08 06:00 [medline] PHST- 2018/08/20 06:00 [entrez] AID - S0304-3940(18)30534-2 [pii] AID - 10.1016/j.neulet.2018.08.004 [doi] PST - ppublish SO - Neurosci Lett. 2018 Oct 15;685:114-123. doi: 10.1016/j.neulet.2018.08.004. Epub 2018 Aug 16.