Figure 8. Working cellular/synaptic model of the role played by NADPH oxidase (NOX) in pLTF.

We postulate that AIH stimulates episodic spinal serotonin (5-HT) release, activating serotonin type 2 (5-HT₂) receptors on phrenic motor neurons (Baker-Herman and Mitchell, 2002). Subsequent activation of protein kinase C (PKC) is postulated to initiate new BDNF synthesis (Baker-Herman et al. 2004) and reactive oxygen species (ROS) formation from NOX activity. We suggest that the ROS inhibit serine/threonine protein phosphatases (PP) that normally constrain pLTF (Wilkerson et al. 2007, 2008; MacFarlane et al. 2008). By inhibiting these phosphatases, the PP constraint is relieved, and pLTF is expressed.