5-HT2A/B receptor expression in the phrenic motor nucleus in a rat model of ALS (SOD1).

Despite respiratory motor neuron death, ventilation is preserved in SOD1 rats. Compensatory respiratory plasticity may counterbalance the loss of these neurons. Phrenic long-term facilitation (pLTF; a form of respiratory plasticity) in naïve rats is 5-HT2 and NADPH oxidase-dependent.

Phrenic long-term facilitation following intrapleural CTB-SAP-induced respiratory motor neuron death.

Amyotrophic lateral sclerosis (ALS) is a devastating disease leading to progressive motor neuron degeneration and death by ventilatory failure. In a rat model of ALS (SOD1), phrenic long-term facilitation (pLTF) following acute intermittent hypoxia (AIH) is enhanced greater than expected at disease end-stage but the mechanism is unknown. We suggest that one trigger for this enhancement is motor neuron death itself.