LTF, a sustained increase in ventilation (VE) after repeated exposure to intermittent hypoxia, is 5HT dependent and is thought to prevent apneas. The sudden infant death syndrome (SIDS) is associated with 5HT deficiency and some SIDS infants had increased and prolonged apneas prior to death. In this study we used the Pet1:flpe ‘silenced’ mouse to test the hypothesis that partial inhibition of 5HT secretion inhibits LTF and leads to increased apneas in early postnatal life. In these mice, the dual activity of Cre and Flpe recombinase activates expression of tetanus toxin light chain in 5HT neurons, which cleaves the VAMP2 protein that anchors synaptic vesicles to the synaptic membrane, thereby inhibiting synaptic vesicular secretion in these neurons. In ‘silenced’ and control pups at postnatal days (P) 5, 8 and 12, we measured VE before, during and after intermittent hypoxia and apnea frequency in the pre‐ and post‐hypoxic periods. VE was normal in ‘silenced’ pups at baseline, but was 10% greater than controls during hypoxia. During the post‐hypoxic period, control pups at P5 and P8 had a 16% and 26% increase in VE normalized to metabolic rate (VE/VO2) respectively, indicative of LTF but VE/VO2 was unchanged in ‘silenced’ pups. The apnea frequency did not change in either genotype during the post‐hypoxic period, despite LTF in control pups. We conclude that in early postnatal life LTF requires 5HT but does not prevent apneas.