 The activated carotid body triggers the release of serotonin that attach to serotonin receptors on the surface of motoneurons, such as the phrenic motoneuron in the case of respiratory recovery.This signal transduction pathway then uses downstream molecules such as TrkB, BDNF, and PKA to increase the synaptic output of the involved motor neuron which in turn increases the motor output of the involved muscles and, thus, decreases functional impairment.As the amount of intermittent hypoxia changes the amount of serotonin release and, as a result, the amount of LTF, this process exhibits metaplasticity.