Circulatory control of phrenic motor plasticity

Acute intermittent hypoxia (AIH) can lead to phrenic motor plasticity through different mechanisms, either by activating brainstem neural networks or by causing local tissue hypoxia in the spinal cord. Moderate AIH activates carotid body chemoreceptors, which in turn stimulate brainstem neural networks and the release of serotonin, leading to phrenic long-term facilitation (pLTF). This process does not depend on tissue hypoxia. Severe AIH, however, triggers a spinal adenosine-dependent mechanism of pLTF, independent of serotonin. Spinal tissue hypoxia is the likely cause, as it leads to the accumulation of extracellular adenosine.

• 1
  Moderate AIH induces serotonin-dependent pLTF, which is independent of tissue hypoxia and relies on carotid body chemoreceptor activation.
• 2
  Severe AIH induces adenosine-dependent pLTF, resulting from spinal tissue hypoxia and extracellular adenosine accumulation.
• 3
  Spinal circulatory control and oxygen delivery play a crucial role in regulating the relative contributions of distinct pathways to phrenic motor plasticity.