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Beth A. Habecker
Researcher at Oregon Health & Science University
Publications - 75
Citations - 1693
Beth A. Habecker is an academic researcher from Oregon Health & Science University. The author has contributed to research in topics: Sympathetic nervous system & Norepinephrine. The author has an hindex of 24, co-authored 62 publications receiving 1330 citations.
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Infarction alters both the distribution and noradrenergic properties of cardiac sympathetic neurons
TL;DR: In the base of the heart, increased TH coupled with no change in NET may explain the increase in extracellular NE observed after MI, and these changes likely contribute to the onset of cardiac arrhythmias.
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Targeting protein tyrosine phosphatase σ after myocardial infarction restores cardiac sympathetic innervation and prevents arrhythmias
Ryan T. Gardner,Lianguo Wang,Bradley T. Lang,Jared M. Cregg,C. L. Dunbar,William R. Woodward,Jerry Silver,Crystal M. Ripplinger,Beth A. Habecker +8 more
TL;DR: Sympathetic reinnervation prevents changes and renders hearts remarkably resistant to induced arrhythmias, and markedly reduces arrhythmia susceptibility following MI.
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The cardiac sympathetic co-transmitter galanin reduces acetylcholine release and vagal bradycardia: Implications for neural control of cardiac excitability
Neil Herring,James Cranley,Michael N. Lokale,Dan Li,Julia Shanks,Eric N. Alston,Beatrice M. Girard,Emma Carter,Rodney L. Parsons,Beth A. Habecker,David J. Paterson +10 more
TL;DR: It is demonstrated that prolonged sympathetic activation releases the slowly diffusing adrenergic co-transmitter galanin in addition to NPY, and that this contributes to the attenuation in vagal bradycardia via a reduction in acetylcholine release.
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Molecular and cellular neurocardiology: development, and cellular and molecular adaptations to heart disease
Beth A. Habecker,Mark E. Anderson,Susan J. Birren,Keiichi Fukuda,Neil Herring,Donald B. Hoover,Hideaki Kanazawa,David J. Paterson,Crystal M. Ripplinger +8 more
TL;DR: This white paper focuses on the cellular and molecular mechanisms that underlie neural–cardiac interactions during development, during normal physiological function in the mature system, and during pathological remodelling in cardiovascular disease.
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Regulation of noradrenergic function by inflammatory cytokines and depolarization
TL;DR: CT‐1 and depolarization regulate expression of noradrenergic properties in an opposing manner, and the combined treatment results in elevated cellular catecholamines and decreased NE uptake relative to control cells.