Volume 1198, Issue 1 p. 252-259
ANNALS OF THE NEW YORK ACADEMY OF SCIENCES

Spinal plasticity following intermittent hypoxia: implications for spinal injury

Erica A. Dale-Nagle

Erica A. Dale-Nagle

Department of Comparative Biosciences, University of Wisconsin, Madison, Wisconsin

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Michael S. Hoffman

Michael S. Hoffman

Department of Comparative Biosciences, University of Wisconsin, Madison, Wisconsin

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Peter M. MacFarlane

Peter M. MacFarlane

Department of Comparative Biosciences, University of Wisconsin, Madison, Wisconsin

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Irawan Satriotomo

Irawan Satriotomo

Department of Comparative Biosciences, University of Wisconsin, Madison, Wisconsin

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Mary Rachael Lovett-Barr

Mary Rachael Lovett-Barr

Department of Comparative Biosciences, University of Wisconsin, Madison, Wisconsin

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Stéphane Vinit

Stéphane Vinit

Department of Comparative Biosciences, University of Wisconsin, Madison, Wisconsin

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Gordon S. Mitchell

Gordon S. Mitchell

Department of Comparative Biosciences, University of Wisconsin, Madison, Wisconsin

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First published: 10 June 2010
Citations: 82
Address for correspondence: Gordon S. Mitchell, Department of Comparative Biosciences, University of Wisconsin, School of Veterinary Medicine, 2215 Linden Avenue, Madison, WI 53706. [email protected]

Abstract

Plasticity is a fundamental property of the neural system controlling breathing. One frequently studied model of respiratory plasticity is long-term facilitation of phrenic motor output (pLTF) following acute intermittent hypoxia (AIH). pLTF arises from spinal plasticity, increasing respiratory motor output through a mechanism that requires new synthesis of brain-derived neurotrophic factor, activation of its high-affinity receptor, tropomyosin-related kinase B, and extracellular-related kinase mitogen-activated protein kinase signaling in or near phrenic motor neurons. Because intermittent hypoxia induces spinal plasticity, we are exploring the potential to harness repetitive AIH as a means of inducing functional recovery in conditions causing respiratory insufficiency, such as cervical spinal injury. Because repetitive AIH induces phenotypic plasticity in respiratory motor neurons, it may restore respiratory motor function in patients with incomplete spinal injury.