Research PaperPhrenic motor neuron TrkB expression is necessary for acute intermittent hypoxia-induced phrenic long-term facilitation

- Acute intermittent hypoxia-induced respiratory motor plasticity requires BDNF signaling.
- Phrenic motor neurons express the high affinity BDNF receptor TrkB.
- Intrapleural siRNA targeting TrkB receptors decreased TrkB receptor expression selectively on phrenic motor neurons.
- Intrapleural siRNA targeting TrkB receptors abolished BDNF dependent, hypoxia-induced respiratory motor plasticity.
- Phrenic motor neurons are a critical site for spinal respiratory motor plasticity.

Phrenic long-term facilitation (pLTF) is a form of hypoxia-induced spinal respiratory motor plasticity that requires new synthesis of brain derived neurotrophic factor (BDNF) and activation of its high-affinity receptor, tropomyosin receptor kinase B (TrkB). Since the cellular location of relevant TrkB receptors is not known, we utilized intrapleural siRNA injections to selectively knock down TrkB receptor protein within phrenic motor neurons. TrkB receptors within phrenic motor neurons are necessary for BDNF-dependent acute intermittent hypoxia-induced pLTF, demonstrating that phrenic motor neurons are a critical site of respiratory motor plasticity.