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Retrograde Neuroanatomical Tracing of Phrenic Motor Neurons in Mice
Published on: February 22, 2018
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Circulatory control of phrenic motor plasticity
Raphael R Perim1, Gordon S Mitchell1
1Center for Respiratory Research and Rehabilitation, Department of Physical Therapy and McKnight Brain Institute, University of Florida, Gainesville, FL, 32610, USA.
Respiratory Physiology & Neurobiology
|January 15, 2019
Summary
Acute intermittent hypoxia (AIH) triggers distinct phrenic motor plasticity pathways. Moderate AIH uses serotonin, while severe AIH relies on spinal adenosine, influenced by local oxygen levels.
Area of Science:
- Neuroscience
- Physiology
Background:
- Acute intermittent hypoxia (AIH) induces phrenic motor plasticity.
- Two distinct mechanisms exist: brainstem-mediated and local spinal cord hypoxia-driven.
Purpose of the Study:
- To review the distinct mechanisms of phrenic motor plasticity.
- To explore the role of local spinal cord circulation and oxygen delivery.
Main Methods:
- Review of existing literature on AIH and phrenic motor plasticity.
- Discussion of chemoreceptor activation, neurotransmitter roles (serotonin, adenosine), and spinal cord circulation.
Main Results:
- Moderate AIH (mAIH) elicits serotonin-dependent phrenic long-term facilitation (pLTF) via carotid body activation.
- Severe AIH (sAIH) evokes adenosine-dependent pLTF, driven by spinal tissue hypoxia.
- Spinal cord circulation compromises shift plasticity towards adenosine.
Conclusions:
- Phrenic motor plasticity is regulated by distinct serotonin and adenosine pathways.
- Local spinal cord oxygen availability and circulation critically influence the dominant plasticity mechanism.
- Neurological disorders affecting spinal circulation may alter phrenic motor plasticity.
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