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NADPH oxidase activity is necessary for phrenic motor facilitation induced by 5HT2B receptor activation

Acute intermittent hypoxia (AIH) elicits phrenic long‐term facilitation (pLTF), a form of respiratory plasticity that requires activation of spinal 5HT2 receptors (Mahamed and Mitchell, 2006). AIH‐induced pLTF requires NADPH oxidase‐derived ROS formation (MacFarlane et al., FASEB J., 2007). Spinal 5‐HT receptor activation in vivo is sufficient to induce phrenic motor facilitation by an NADPH oxidase‐dependent mechanism, but the specific 5‐HT receptor subtypes involved are not known. In this study, we tested 1) whether spinal 5‐HT2B receptor activation is sufficient to elicit phrenic motor facilitation (without hypoxia), and 2) whether phrenic motor facilitation following 5‐HT2B receptor activation requires spinal NADPH oxidase activity. In anesthetized, paralyzed and ventilated rats with constant arterial PO2 and PCO2, episodic intrathecal (i.t.) injections of 5‐HT (1mM) at C4 (5μl, 3 injections, 5min intervals) or the selective 5‐HT2B receptor agonist BW723C86 (1mM) both elicited significant phrenic motor facilitation at 60min post‐injections. Pre‐treatment with a single i.t. injection of apocynin (600μM, 12μl, i.t.), an NADPH oxidase inhibitor, blocked phrenic motor facilitation induced by both 5‐HT and BW723C86. Thus, episodic spinal 5‐HT2B receptor activation is sufficient to elicit phrenic motor facilitation in vivo by a mechanism that requires spinal NADPH oxidase activity. These findings sugest that 5‐HT2B receptors contribute to serotonin‐dependent phrenic motor facilitation (including AIH‐induced pLTF) by an NADPH oxidase dependent mechanism.