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Cardioprotection induced in a mouse model of neuropathic pain via anterior nucleus of paraventricular thalamus

Yi-Fen Cheng, Ya-Ting Chang, Wei-Hsin Chen, Hsi-Chien Shih, Yen-Hui Chen, Bai-Chuang Shyu and Chien-Chang Chen ()
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Yi-Fen Cheng: Graduate Institute of Life Sciences, National Defense Medical Center
Ya-Ting Chang: Institute of Biomedical Sciences, Academia Sinica
Wei-Hsin Chen: Institute of Biomedical Sciences, Academia Sinica
Hsi-Chien Shih: Institute of Biomedical Sciences, Academia Sinica
Yen-Hui Chen: Institute of Biomedical Sciences, Academia Sinica
Bai-Chuang Shyu: Institute of Biomedical Sciences, Academia Sinica
Chien-Chang Chen: Graduate Institute of Life Sciences, National Defense Medical Center

Nature Communications, 2017, vol. 8, issue 1, 1-16

Abstract: Abstract Myocardial infarction is the leading cause of death worldwide. Restoration of blood flow rescues myocardium but also causes ischemia-reperfusion injury. Here, we show that in a mouse model of chronic neuropathic pain, ischemia-reperfusion injury following myocardial infarction is reduced, and this cardioprotection is induced via an anterior nucleus of paraventricular thalamus (PVA)-dependent parasympathetic pathway. Pharmacological inhibition of extracellular signal-regulated kinase activation in the PVA abolishes neuropathic pain-induced cardioprotection, whereas activation of PVA neurons pharmacologically, or optogenetic stimulation, is sufficient to induce cardioprotection. Furthermore, neuropathic injury and optogenetic stimulation of PVA neurons reduce the heart rate. These results suggest that the parasympathetic nerve is responsible for this unexpected cardioprotective effect of chronic neuropathic pain in mice.

Date: 2017
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DOI: 10.1038/s41467-017-00891-z

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