Phrenic long-term facilitation requires PKCθ activity within phrenic motor neurons.

Acute intermittent hypoxia (AIH) induces a form of spinal motor plasticity known as phrenic long-term facilitation (pLTF); pLTF is a prolonged increase in phrenic motor output after AIH has ended. In anesthetized rats, we demonstrate that pLTF requires activity of the novel isoform, and that the relevant is within phrenic motor neurons. Whereas spinal duanyu1531θ inhibitors block pLTF, inhibitors targeting other duanyu1531 isoforms do not. duanyu1531θ is highly expressed in phrenic motor neurons, and duanyu1531θ knockdown with intrapleural siRNAs abolishes pLTF. Intrapleural siRNAs targeting an atypical duanyu1531 isoform expressed in phrenic motor neurons that underlies a distinct form of phrenic motor plasticity, does not affect pLTF. Thus, duanyu1531θ plays a critical role in spinal AIH-induced respiratory motor plasticity, and the relevant duanyu1531θ is localized within phrenic motor neurons. Intrapleural siRNA delivery has considerable potential as a therapeutic tool to selectively manipulate plasticity in vital respiratory motor neurons.

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